Journal articles on the topic 'GFAP biomarker'
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Huss, André, Ahmed Abdelhak, Benjamin Mayer, Hayrettin Tumani, Hans-Peter Müller, Katharina Althaus, Jan Kassubek, et al. "Association of Serum GFAP with Functional and Neurocognitive Outcome in Sporadic Small Vessel Disease." Biomedicines 10, no. 8 (August 2, 2022): 1869. http://dx.doi.org/10.3390/biomedicines10081869.
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Cerebrospinal fluid (CSF) and serum biomarkers are critical for clinical decision making in neurological diseases. In cerebral small vessel disease (CSVD), white matter hyperintensities (WMH) are an important neuroimaging biomarker, but more blood-based biomarkers capturing different aspects of CSVD pathology are needed. In 42 sporadic CSVD patients, we prospectively analysed WMH on magnetic resonance imaging (MRI) and the biomarkers neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), chitinase3-like protein 1 (CHI3L1), Tau and Aβ1-42 in CSF and NfL and GFAP in serum. GFAP and CHI3L1 expression was studied in post-mortem brain tissue in additional cases. CSVD cases with higher serum NfL and GFAP levels had a higher modified Rankin Scale (mRS) and NIHSS score and lower CSF Aβ1-42 levels, whereas the CSF NfL and CHI3L1 levels were positively correlated with the WMH load. Moreover, the serum GFAP levels significantly correlated with the neurocognitive functions. Pathological analyses in CSVD revealed a high density of GFAP-immunoreactive fibrillary astrocytic processes in the periventricular white matter and clusters of CHI3L1-immunoreactive astrocytes in the basal ganglia and thalamus. Thus, besides NfL, serum GFAP is a highly promising fluid biomarker of sporadic CSVD, because it does not only correlate with the clinical severity but also correlates with the cognitive function in patients.
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Högel, Heidi, Eero Rissanen, Christian Barro, Markus Matilainen, Marjo Nylund, Jens Kuhle, and Laura Airas. "Serum glial fibrillary acidic protein correlates with multiple sclerosis disease severity." Multiple Sclerosis Journal 26, no. 2 (December 20, 2018): 210–19. http://dx.doi.org/10.1177/1352458518819380.
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Background: Cerebrospinal fluid (CSF) levels of two soluble biomarkers, glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL), have been shown to associate with multiple sclerosis (MS) disease progression. Now, both biomarkers can be detected reliably in serum, and importantly, their serum levels correlate well with their CSF levels. Objective: To evaluate the usability of serum GFAP measurement as a biomarker of progressive disease and disease severity in MS. Methods: Clinical course, Expanded Disability Status Scale (EDSS), disease duration, patient age and magnetic resonance imaging (MRI) parameters were reviewed in 79 MS patients in this cross-sectional hospital-based study. Serum samples were collected for measurement of GFAP and NfL concentrations using single molecule array (Simoa) assay. A cohort of healthy controls was evaluated for comparison. Results: Higher serum concentrations of both GFAP and NfL were associated with higher EDSS, older age, longer disease duration, progressive disease course and MRI pathology. Conclusion: Earlier studies have demonstrated that GFAP, unlike NfL, is not increased in association with acute focal inflammation-related nervous system damage. Our work suggests that GFAP serum level associates with disease progression in MS and could potentially serve as an easily measurable biomarker of central nervous system (CNS) pathology related to disease progression in MS.
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Bustamante, Alejandro, Anna Penalba, Cyrille Orset, Leire Azurmendi, Víctor Llombart, Alba Simats, Emili Pecharroman, et al. "Blood Biomarkers to Differentiate Ischemic and Hemorrhagic Strokes." Neurology 96, no. 15 (March 5, 2021): e1928-e1939. http://dx.doi.org/10.1212/wnl.0000000000011742.
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ObjectiveTo validate a panel of blood biomarkers to differentiate between ischemic stroke (IS) and intracerebral hemorrhage (ICH) in patients with suspected stroke.MethodsPatients with suspected stroke admitted within 4.5 hours after onset were enrolled. Blood samples were collected at hospital admission. Glial fibrillary acid protein (GFAP), retinol binding protein 4 (RBP-4), N-terminal proB-type natriuretic peptide (NT-proBNP), and endostatin were measured by immunoassays. Cutoff points were obtained for 100% specificity for IS. A high-sensitivity assay to measure GFAP and rapid point-of-care tests (POCTs) to measure RBP-4 and NT-proBNP were used in subsets of patients. Biomarker panels were evaluated in another cohort of 62 stroke mimics.ResultsA total of 189 patients (154 IS and 35 ICH) were enrolled. Patients with IS had higher RBP-4, NT-proBNP, and endostatin and lower GFAP levels than patients with ICH. The best biomarker combination for the identification of IS was RBP-4+NT-proBNP, which was able to identify 29.7% of patients with IS with 100% specificity. In the subset of patients for whom GFAP was measured with the high-sensitivity assay, RBP-4, NT-proBNP, and GFAP identified 51.5% of patients with IS with 100% specificity. When stroke mimics were included, specificities were reduced to 98.4 and 96.8%, respectively. POCTs of RBP-4 and NT-proBNP showed results similar results to those of conventional ELISAs.ConclusionsA biomarker panel including RBP-4, NT-proBNP, and GFAP provided moderate but potentially useful sensitivity rates at 100% specificity for IS diagnosis. If confirmed in future studies, this strategy might allow prehospital treatment in selected patients.Classification of EvidenceThis study provides Class I evidence that a biomarker panel including RBP-4, NT-proBNP, and GFAP distinguishes IS from ICH with moderate accuracy.
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Halford, Julia, Sean Shen, Kyohei Itamura, Jaclynn Levine, Albert C. Chong, Gregg Czerwieniec, Thomas C. Glenn, et al. "New astroglial injury-defined biomarkers for neurotrauma assessment." Journal of Cerebral Blood Flow & Metabolism 37, no. 10 (August 17, 2017): 3278–99. http://dx.doi.org/10.1177/0271678x17724681.
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Traumatic brain injury (TBI) is an expanding public health epidemic with pathophysiology that is difficult to diagnose and thus treat. TBI biomarkers should assess patients across severities and reveal pathophysiology, but currently, their kinetics and specificity are unclear. No single ideal TBI biomarker exists. We identified new candidates from a TBI CSF proteome by selecting trauma-released, astrocyte-enriched proteins including aldolase C (ALDOC), its 38kD breakdown product (BDP), brain lipid binding protein (BLBP), astrocytic phosphoprotein (PEA15), glutamine synthetase (GS) and new 18-25kD-GFAP-BDPs. Their levels increased over four orders of magnitude in severe TBI CSF. First post-injury week, ALDOC levels were markedly high and stable. Short-lived BLBP and PEA15 related to injury progression. ALDOC, BLBP and PEA15 appeared hyper-acutely and were similarly robust in severe and mild TBI blood; 25kD-GFAP-BDP appeared overnight after TBI and was rarely present after mild TBI. Using a human culture trauma model, we investigated biomarker kinetics. Wounded (mechanoporated) astrocytes released ALDOC, BLBP and PEA15 acutely. Delayed cell death corresponded with GFAP release and proteolysis into small GFAP-BDPs. Associating biomarkers with cellular injury stages produced astroglial injury-defined (AID) biomarkers that facilitate TBI assessment, as neurological deficits are rooted not only in death of CNS cells, but also in their functional compromise.
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Borko, Tyler L., Britney Barrera, Christopher Mizenko, Aurélie Ledreux, Ryan Kammeyer, Alanna Ritchie, Sean Selva, et al. "Examining the Differences in Biomarkers of Neuronal and Glial Injury Between Autoimmune Neurologic Disease Patients and Healthy Controls." Neurology 99, no. 23 Supplement 2 (December 5, 2022): S8—S9. http://dx.doi.org/10.1212/01.wnl.0000903096.36040.1d.
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ObjectiveTo evaluate differences in concentrations of serum-based biomarkers obtained from a screened healthy control (HC) population compared to age and sex matched autoimmune and inflammatory neurologic disease (AIND) patients.BackgroundProtein markers of neuronal and glial injury have become important, minimally invasive biomarkers for understanding the impact of disease in various neurological disorders, including ongoing research into AINDs. Levels of these proteins in healthy individuals remain unclear.Design/MethodsNeurofilament light (NfL), glial fibrillary acidic protein (GFAP), ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1), and total tau (Tau) levels in AIND and HC participants will be compared. Multiple Sclerosis (MS) patients, as inflammatory controls, will be analyzed as well. AIND and HC participant serum samples have been collected to obtain NfL, GFAP, UCH-L1, and Tau protein levels using Quanterix SR-XTM SIMOA. We plan to analyze and compare age and sex matched HC samples to AIND patients for each biomarker, ages ranging from 20-80 years old. Concentrations will be log transformed and analyzed with mixed model regression.ResultsHealthy Controls (130), AIND (255), and newly diagnosed/treatment naïve MS samples (681) have already been collected. Nineteen HC and AIND (includes NMDA, LGI1, TRIM46, CRMP5, MOG, DPPX, GABA-A, GAD-65) participants were analyzed. Preliminary results for HC show mean Nfl (10.3 pg/mL), GFAP (78.9 pg/mL), UCH-L1 (5.65 pg/mL), and Tau (0.53 pg/mL) levels, and for AIND patients mean Nfl (186.48 pg/mL), GFAP (434.92 pg/mL), UCH-L1 (71.38 pg/mL), and Tau (51.85 pg/mL) levels. While ongoing biomarker analysis will be completed with HC that are age and sex matched, the significantly higher levels in AIND patients highlights the importance of creating baseline values in HC to understand these same biomarkers in AIND patients.ConclusionsPreliminary results show NfL and GFAP levels are significantly higher in AIND patients versus HC. Baseline biomarker values are essential for understanding further research in biomarkers related to AIND.
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Ganne, Akshatha, Meenakshisundaram Balasubramaniam, W. Sue T. Griffin, Robert J. Shmookler Reis, and Srinivas Ayyadevara. "Glial Fibrillary Acidic Protein: A Biomarker and Drug Target for Alzheimer’s Disease." Pharmaceutics 14, no. 7 (June 26, 2022): 1354. http://dx.doi.org/10.3390/pharmaceutics14071354.
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Glial fibrillary acidic protein (GFAP) is an intermediate filament structural protein involved in cytoskeleton assembly and integrity, expressed in high abundance in activated glial cells. GFAP is neuroprotective, as knockout mice are hypersensitive to traumatic brain injury. GFAP in cerebrospinal fluid is a biomarker of Alzheimer’s disease (AD), dementia with Lewy bodies, and frontotemporal dementia (FTD). Here, we present novel evidence that GFAP is markedly overexpressed and differentially phosphorylated in AD hippocampus, especially in AD with the apolipoprotein E [ε4, ε4] genotype, relative to age-matched controls (AMCs). Kinases that phosphorylate GFAP are upregulated in AD relative to AMC. A knockdown of these kinases in SH-SY5Y-APPSw human neuroblastoma cells reduced amyloid accrual and lowered protein aggregation and associated behavioral traits in C. elegans models of polyglutamine aggregation (as observed in Huntington’s disease) and of Alzheimer’s-like amyloid formation. In silico screening of the ChemBridge structural library identified a small molecule, MSR1, with stable and specific binding to GFAP. Both MSR1 exposure and GF AP-specific RNAi knockdown reduce aggregation with remarkably high concordance of aggregate proteins depleted. These data imply that GFAP and its phosphorylation play key roles in neuropathic aggregate accrual and provide valuable new biomarkers, as well as novel therapeutic targets to alleviate, delay, or prevent AD.
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Zwirner, Johann, Simone Bohnert, Heike Franke, Jack Garland, Niels Hammer, Dustin Möbius, Rexson Tse, and Benjamin Ondruschka. "Assessing Protein Biomarkers to Detect Lethal Acute Traumatic Brain Injuries in Cerebrospinal Fluid." Biomolecules 11, no. 11 (October 25, 2021): 1577. http://dx.doi.org/10.3390/biom11111577.
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Diagnosing traumatic brain injury (TBI) from body fluids in cases where there are no obvious external signs of impact would be useful for emergency physicians and forensic pathologists alike. None of the previous attempts has so far succeeded in establishing a single biomarker to reliably detect TBI with regards to the sensitivity: specificity ratio in a post mortem setting. This study investigated a combination of body fluid biomarkers (obtained post mortem), which may be a step towards increasing the accuracy of biochemical TBI detection. In this study, serum and cerebrospinal fluid (CSF) samples from 30 acute lethal TBI cases and 70 controls without a TBI-related cause of death were evaluated for the following eight TBI-related biomarkers: brain-derived neurotrophic factor (BDNF), ferritin, glial fibrillary acidic protein (GFAP), interleukin 6 (IL-6), lactate dehydrogenase, neutrophil gelatinase-associated lipocalin (NGAL), neuron-specific enolase and S100 calcium-binding protein B. Correlations among the individual TBI biomarkers were assessed, and a specificity-accentuated threshold value analysis was conducted for all biomarkers. Based on these values, a decision tree modelling approach was performed to assess the most accurate biomarker combination to detect acute lethal TBIs. The results showed that 92.45% of acute lethal TBIs were able to be diagnosed using a combination of IL-6 and GFAP in CSF. The probability of detecting an acute lethal TBI was moderately increased by GFAP alone and considerably increased by the remaining biomarkers. BDNF and NGAL were almost perfectly correlated (p = 0.002; R2 = 0.944). This study provides evidence that acute lethal TBIs can be detected to a high degree of statistical accuracy using forensic biochemistry. The high inter-individual correlations of biomarkers may help to estimate the CSF concentration of an unknown biomarker, using extrapolation techniques.
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Savage, William J., Zongming Fu, Emily Barron-Casella, Pratima Dulloor, Jacky Jennings, Elizabeth Dackiw, Kimberly Jones, et al. "Glial Fibrillary Acidic Protein as a Plasma Biomarker of Brain Injury in Children with Sickle Cell Disease." Blood 114, no. 22 (November 20, 2009): 1512. http://dx.doi.org/10.1182/blood.v114.22.1512.1512.
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Abstract Abstract 1512 Poster Board I-535 Introduction In children with sickle cell disease (SCD), silent cerebral infarct (SCI) is an independent risk factor for lower IQ, poorer school performance, and overt stroke. MRI is the only method to identify patients with SCI. A blood biomarker of SCI in patients with sickle cell disease (SCD) would fill a clinical void because blood is easy to obtain and measure, a biomarker may determine risk of or progression of neurologic injury to overt stroke, and a biomarker could benchmark current and new therapies for SCI and other subclinical forms of neurologic injury in SCD. We hypothesized that an unbiased proteomics screen of plasma from sickle cell patients would yield biomarkers of brain injury. Methods A cross-sectional sample of children 5-14 years old with sickle cell disease (HbSS and HbSB0) who were screened for the Silent Infarct Transfusion (SIT) Trial (ClinicalTrials.gov NCT00072761) were studied (n=258) along with 60 age-matched healthy controls and 28 adults with overt brain injury. For biomarker discovery, plasma underwent depletion of hemoglobin with nickel- nitrilotriacetic acid and immunoaffinity depletion of the 12 most abundant plasma proteins. After fractionation by reverse phase liquid chromatography over a C18 column and acetonitrile gradient and trypsin digestion, peptide spectra from each fraction were obtained by LC/MS/MS (LTQ-Orbitrap) and were searched using X!Tandem and human IPI database version 3.5. Post search analysis was performed using Proteomics Analysis Software System (Integrated Analysis Inc., Bethesda, MD). An electrochemiluminescent immunoassay was developed for one of the candidate proteins identified, glial fibrillary acidic protein (GFAP), for protein validation (MesoScale Discovery). Results GFAP, a brain-specific intermediate filament known to be a marker of acute stroke and head trauma in adults, was identified in discovery sample plasma. Four percent of sickle cell subjects in steady-state had plasma GFAP concentrations similar to stroke and brain surgery controls (>0.45 ng/mL). Among sickle cell subjects 5-14 years old screened for the SIT Trial, 9.3% had GFAP concentrations above the 95th percentile of age-matched controls (95th percentile cutoff: 0.227 ng/mL; p=0.08). Sickle cell subjects with silent cerebral infarct (SCI) had more elevations above the normal 95th percentile (10/69; 14.5%) than those without SCI (9/131; 6.8%), although this difference was not statistically significant (p=0.08). The sensitivity of GFAP as a marker of brain injury was demonstrated in a case of an 11 year-old child with HbSS and acute stroke in which plasma GFAP was 1.52 ng/mL (6 times the normal control 95th percentile) before the stroke was clinically evident and peaked at 2.83 ng/mL. We discovered GFAP as a circulating brain protein in plasma of children with SCD. Plasma GFAP is a marker of acute stroke in sickle cell disease but discriminates only minimally between SCI and non-SCI status in the SIT Trial using baseline cross-sectional samples. Four percent of children with sickle disease 5-14 years old have plasma GFAP levels similar to controls with severe brain injury without clinical evidence of overt stroke. Conclusions Elevations in circulating brain proteins such as GFAP show promise as indicators of subacute brain injury in children with SCI, but will require longitudinal studies of plasma GFAP in children with SCI to clarify the utility of GFAP as a plasma biomarker of SCI and a predictor of neurologic risk. Disclosures No relevant conflicts of interest to declare.
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Chaykovskaya, A. D., M. P. Topuzova, A. M. Makhanova, A. G. Mikheeva, D. S. Korotkova, M. L. Pospelova, E. B. Panina, et al. "Role of neuron-specific enolase, glial fibrillar acidic protein and NR2-antibodies in early diagnostic of ischemic stroke." Translational Medicine 8, no. 5 (December 18, 2021): 5–20. http://dx.doi.org/10.18705/2311-4495-2021-8-5-5-20.
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Background. Application of a biomarker panel during the acute period of the ischemic stroke (IS) can contribute to a more accurate and prompter diagnostics and verification of the optimal approach to a patients’ management.Objective. We aimed to clarify values of neuron-specific enolase (NSE), glial fibrillar acidic protein (GFAP) and antibodies for NMDA receptor’s NR2-subunit (NR2-antibodies) in the acute period of IS, to compare with such values in patients without IS, to assess their relationship with severity of neurological deficit and short-term outcome and also to establish sensitivity and specificity of the biomarker panel.Design and methods. 63 patients with IS and 31 people (11 with chronic brain ischemia and 20 healthy individuals) as controls were included. Results. NSE and GFAP values in IS group exceeded reference values at the onset of disease, lowering significally by 10-14 day, while NR2-antibodies’ values were lower at the onset of the disease compared with controls, rising by 10-14 day. In patients with unfavourable short-term outcome higher levels of NSE, GFAP and NR2-antibodies were found. A panel of such biomarkers has higher sensitivity and specificity than each of them individually.Conclusion. Researched substances can be used in a biomarker panel for IS diagnostics, brain damage monitoring, patient’s condition evaluation and short outcome prognosing.
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Ebenau, Jarith L., Wiesje Pelkmans, Inge M. W. Verberk, Sander C. J. Verfaillie, Karlijn A. van den Bosch, Mardou van Leeuwenstijn, Lyduine E. Collij, et al. "Association of CSF, Plasma, and Imaging Markers of Neurodegeneration With Clinical Progression in People With Subjective Cognitive Decline." Neurology 98, no. 13 (February 2, 2022): e1315-e1326. http://dx.doi.org/10.1212/wnl.0000000000200035.
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Background and ObjectivesMultiple biomarkers have been suggested to measure neurodegeneration (N) in the AT(N) framework, leading to inconsistencies between studies. We investigated the association of 5 N biomarkers with clinical progression and cognitive decline in individuals with subjective cognitive decline (SCD).MethodsWe included individuals with SCD from the Amsterdam Dementia Cohort and SCIENCe project, a longitudinal cohort study (follow-up 4±3 years). We used the following N biomarkers: CSF total tau (t-tau), medial temporal atrophy visual rating on MRI, hippocampal volume (HV), serum neurofilament light (NfL), and serum glial fibrillary acidic protein (GFAP). We determined correlations between biomarkers. We assessed associations between N biomarkers and clinical progression to mild cognitive impairment or dementia (Cox regression) and Mini-Mental State Examination (MMSE) over time (linear mixed models). Models included age, sex, CSF β-amyloid (Aβ) (A), and CSF p-tau (T) as covariates, in addition to the N biomarker.ResultWe included 401 individuals (61±9 years, 42% female, MMSE 28 ± 2, vascular comorbidities 8%–19%). N biomarkers were modestly to moderately correlated (range r −0.28 – 0.58). Serum NfL and GFAP correlated most strongly (r 0.58, p < 0.01). T-tau was strongly correlated with p-tau (r 0.89, p < 0.01), although these biomarkers supposedly represent separate biomarker groups. All N biomarkers individually predicted clinical progression, but only HV, NfL, and GFAP added predictive value beyond Aβ and p-tau (hazard ratio 1.52 [95% CI 1.11–2.09]; 1.51 [1.05–2.17]; 1.50 [1.04–2.15]). T-tau, HV, and GFAP individually predicted MMSE slope (range β −0.17 to −0.11, p < 0.05), but only HV remained associated beyond Aβ and p-tau (β −0.13 [SE 0.04]; p < 0.05).DiscussionIn cognitively unimpaired older adults, correlations between different N biomarkers were only moderate, indicating they reflect different aspects of neurodegeneration and should not be used interchangeably. T-tau was strongly associated with p-tau (T), which makes it less desirable to use as a measure for N. HV, NfL, and GFAP predicted clinical progression beyond A and T. Our results do not allow to choose one most suitable biomarker for N, but illustrate the added prognostic value of N beyond A and T.Classification of EvidenceThis study provides Class II evidence that HV, NfL, and GFAP predicted clinical progression beyond A and T in individuals with SCD.
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Tan, Chengbing, Min Zhong, Zhengxiong Yao, Siqi Hong, Li Jiang, and Yan Jiang. "Anti-GFAP Antibody-Associated Hypertrophic Pachymeningitis." Neuropediatrics 53, no. 02 (February 11, 2022): 143–45. http://dx.doi.org/10.1055/s-0042-1742718.
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Abstract Background Autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy is an inflammatory central nervous system (CNS) disorder that usually presents as steroid responsive encephalitis, meningitis, myelitis, or meningoencephalomyelitis. Hypertrophic pachymeningitis (HP) is an uncommon disorder that causes a localized or diffuse thickening of the dura mater. Depending on the etiology, HP can be idiopathic or secondary to a wide variety of other diseases. There are no reports of autoimmune GFAP astrocytopathy presenting as HP. Methods In this case report, we describe a rare case of pediatric HP possibly associated with anti-GFAP antibody. Results A 13-year-old previously healthy girl presented with headache for nearly 8 months with left-sided peripheral facial palsy and left-sided abductor nerve palsy in the second month of course. Magnetic resonance imaging (MRI) of the brain revealed contrast enhancement of hypertrophic dura mater. Anti-GFAPα antibodies were positive in serum and cerebrospinal fluid. The patient improved clinically after steroid treatment with partial resolution of abnormal intracranial MRI lesions. Conclusion The present study suggests that HP may be one of the clinical phenotypes for autoimmune GFAP astrocytopathy or GFAP antibody is a biomarker for HP.
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Wei, Yuzhen, Haoxiao Chang, Xindi Li, Li Du, Wangshu Xu, Hengri Cong, Yajun Yao, Xinghu Zhang, and Linlin Yin. "CSF-S100B Is a Potential Candidate Biomarker for Neuromyelitis Optica Spectrum Disorders." BioMed Research International 2018 (October 22, 2018): 1–11. http://dx.doi.org/10.1155/2018/5381239.
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Astrocytic impairment is a pathologic feature of neuromyelitis optica spectrum disorder (NMOSD). S100B and glial fibrillary acidic protein (GFAP) are the two most commonly used astrocytic markers. The aim of this study was to evaluate whether CSF-S100B could serve as a marker of NMOSD. We enrolled 49 NMOSD patients [25 aquaporin-4 antibody (AQP4-Ab)–positive, 8 myelin-oligodendrocyte glycoprotein antibody (MOG-Ab)-positive, and 16 seronegative patients], 12 multiple sclerosis (MS) patients, and 15 other noninflammatory neurological diseases (OND) patients. The CSF levels of S100B and GFAP were measured by ELISA. Both CSF-S100B and GFAP levels significantly discriminated NMOSD from MS [area under curve (AUC) = 0.839 and 0.850, respectively] and OND (AUC = 0.839 and 0.850, respectively). The CSF-S100B levels differentiated AQP4-Ab–positive NMOSD from MOG-Ab–positive NMOSD with higher accuracy than the CSF-GFAP levels (AUC=0.865 and 0.772, respectively). The CSF-S100B levels also significantly discriminated MOG-Ab–positive patients from seronegative patients (AUC = 0.848). Both CSF-S100B and GFAP levels were correlated with the Expanded Disability Status Scale (EDSS) during remission. Only the CSF-S100B levels were correlated with the CSF WBC count and the EDSS during attack. The levels of CSF-S100B seemed to have a longer lasting time than the levels of CSF-GFAP, which may benefit patients who present late. As a result, CSF-S100B might be a potential candidate biomarker for NMOSD in discriminating, evaluating severity, and predicting disability.
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Priambada, Dody, Muhamad Thohar Arifin, Surya Pratama Briliantika, Dian Widyaningrum, Abdi Saputro, Azka Tajussyarof El Muzakka, Yuriz Bakhtiar, Krisna Tsaniadi Prihastomo, and Zainal Muttaqin. "Serum GFAP and EGFR as Supportive Diagnostic Biomarker of Glioma Patients: A Single-Center Study." Open Access Macedonian Journal of Medical Sciences 10, B (April 20, 2022): 1093–96. http://dx.doi.org/10.3889/oamjms.2022.9021.
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Background : High grade Gliomas (HGGs) (World Health Organization grade III and IV) are aggressive brain tumors with a poor prognosis. Serum concentrations of GFAP and EGFR are theoretically raised in glioma patients, especially primary HGGs
Aim : To look at serum levels of GFAP and EGFR in patients with Gliomas (Low Grade and High-Grade Glioma) and see if they were related to clinical outcome, MRI parameter and pathological features.
Method : Between 2020-2021, pre-operative blood samples were taken from 39 patients with radiologically diagnosed glioma who were performed for tumour excision. The time between blood collection and surgical resection was an average of 10 days. GFAP and EGFR serum were compared in glioma and non-glioma patients.
Result : Glioma patients had average of serum GFAP 747.93 + 1349.49 pg/ml and average of Serum EGFR 9.25 + 3.17 ng/ml. Non glioma average of GFAP and EGFR respectively were 292.91 + 369.30 pg/ml and 7.81 + 3.38 ng/ml.From all variable, we performed normality test using the Saphiro-wilk normality test and all variable were no normally distribution with p<0.05
Conclusion : Circulating GFAP and EGFR are promising method for “supportive” methods for differentiate between glioma and non-glioma patients, especially high grade glioma
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Kassubek, Rebecca, Martin Gorges, Michael Schocke, Viktoria A. M. Hagenston, André Huss, Albert C. Ludolph, Jan Kassubek, and Hayrettin Tumani. "GFAP in early multiple sclerosis: A biomarker for inflammation." Neuroscience Letters 657 (September 2017): 166–70. http://dx.doi.org/10.1016/j.neulet.2017.07.050.
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Müller, Thomas. "GFAP, NFL und Kappa-Leichtketten: Biomarker für frühe MS." InFo Neurologie + Psychiatrie 24, no. 11 (November 2022): 51–52. http://dx.doi.org/10.1007/s15005-022-3083-9.
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Gasso, V. Y., A. N. Hahut, S. V. Yermolenko, I. A. Hasso, C. A. Agca, E. V. Sukharenko, and V. S. Nedzvetsky. "Local industrial pollution induces astrocyte cytoskeleton rearrangement in the dice snake brain: GFAP as a biomarker." Biosystems Diversity 28, no. 3 (July 18, 2020): 250–56. http://dx.doi.org/10.15421/012033.
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The present study was designed to evaluate the responsiveness of modulation of glial fibrillary acidic protein (GFAP) content and its fragmentation in the snake brain as a biomarker of local industrial pollution of aquatic ecosystems. Despite GFAP being a well known cytoskeleton marker of astrocytes’ reactivity in the brain of vertebrates, its expression in the snake brain remains insufficiently described. The GFAP expression and its fragmentation were detected using the immunoblot method in the snake brain. ROS level was determined with dichlorofluorescein diacetate fluorescence. The content of the glial fibrillary acidic protein (GFAP) of filament (cytoskeleton) and soluble (cytosol) fractions in the brain of dice snake Natrix tessellata from three ecosystems with different rates of industrial pollution were studied (two polluted and one clean control site). Characteristic increase in GFAP fragmentation was noted for the snakes from both the researched polluted sites. Significant increase in the content of the GFAP cleaved polypeptide fragments induced by industrial pollution exposure was confirmed in the snakes’ brains. Meaningful GFAP fragmentation was determined in snake brain astrocytes as an increase in cleaved fragments of 47–35 kDa molecular weight for both soluble and cytoskeletal GFAP fractions. We found significant abnormality in the ratio of the GFAP soluble fraction to the cytoskeletal one in contaminant-exposed dice snakes. It should testify to significant metabolic disturbance in nerve cells of the dice snakes. Furthermore, growth of reactive oxygen species level as the main cause of oxidative stress was determined in brains of the snakes exposed to environmental toxicity. Thus, astrocyte cytoskeleton disorders are associated with pollutant-induced redox imbalance in the snake brain. Despite the limited data on glial cell biology in the reptilian brain, the observed results prove that snake astrocytes can respond to the environmental toxicity using typical astroglial response. The presented results evidence that monitoring of molecular characteristics of glial cytoskeleton in dice snakes could be used as reliable biomarker of neurotoxicity and adverse effects of industrial pollution. Further studies are required to elucidate the role of astrocyte cytoskeleton in the response against neurotoxic contaminants.
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Sarkis, George Anis, Tian Zhu, Zhihui Yang, Xue Li, Yuan Shi, Richard Rubenstein, Richard A. Yost, Geoffrey T. Manley, and Kevin K. Wang. "Characterization and standardization of multiassay platforms for four commonly studied traumatic brain injury protein biomarkers: a TBI Endpoints Development Study." Biomarkers in Medicine 15, no. 18 (December 2021): 1721–32. http://dx.doi.org/10.2217/bmm-2021-0284.
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Aim: There is a critical need to validate biofluid-based biomarkers as diagnostic and drug development tools for traumatic brain injury (TBI). As part of the TBI Endpoints Development Initiative, we identified four potentially predictive and pharmacodynamic biomarkers for TBI: astroglial markers GFAP and S100B and the neuronal markers UCH-L1 and Tau. Materials & methods: Several commonly used platforms for these four biomarkers were identified and compared on analytic performance and ability to detect gold standard recombinant protein antigens and to pool control versus TBI cerebrospinal fluid (CSF). Results: For each marker, only some assay formats could differentiate TBI CSF from the control CSF. Also, different assays for the same biomarker reported divergent biomarker values for the same biosamples. Conclusion: Due to the variability of TBI marker assay in performance and reported values, standardization strategies are recommended when comparing reported biomarker levels across assay platforms.
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Gao, Ning, Xiaohui Zhang-Brotzge, Bushra Wali, Iqbal Sayeed, Joshua J. Chern, Laura S. Blackwell, Chia-Yi Kuan, and Andrew Reisner. "Plasma osteopontin may predict neuroinflammation and the severity of pediatric traumatic brain injury." Journal of Cerebral Blood Flow & Metabolism 40, no. 1 (March 13, 2019): 35–43. http://dx.doi.org/10.1177/0271678x19836412.
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Traumatic brain injury (TBI) is the leading cause of death in children and adolescents in developed countries, but there are no blood-based biomarkers to support the diagnosis or prognosis of pediatric TBI to-date. Here we report that the plasma levels of osteopontin (OPN), a phosphoprotein chiefly secreted by macrophages and/or activated microglia, may contribute to this goal. In animal models of TBI, while OPN, fibrillary acidic protein (GFAP), and matrix metalloproteinase 9 (MMP-9) were all readily induced by controlled cortical impact in the brains of one-month-old mice, only OPN and GFAP ascended in the blood in correlation with high neurological severity scores (NSS). In children with TBI (three to nine years of age, n = 66), the plasma levels of OPN, but not GFAP, correlated with severe TBI (Glasgow Coma Score ≤ 8) and intracranial lesions at emergency department. In addition, the plasma OPN levels in severe pediatric TBI patients continued to ascend for 72 h and correlated with mortality and the days requiring ventilator or intensive care unit support, whereas the plasma GFAP levels lacked these properties. Together, these results suggest that plasma OPN outperforms GFAP and may be a neuroinflammation-based diagnostic and prognostic biomarker in pediatric TBI.
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Senaratne, Nipuna, Alexandra Hunt, Eleanor Sotsman, and Michael J. Grey. "Biomarkers to aid the return to play decision following sports-related concussion: a systematic review." Journal of Concussion 6 (January 2022): 205970022110707. http://dx.doi.org/10.1177/20597002211070735.
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Premature return to play (RTP) following sports-related concussion (SRC) is associated with significant morbidity including risk of neurological and non-neurological injury, persistent post-concussion symptoms and chronic neurological deficits. Assessing athletes for RTP is critical but these decisions are currently based on clinical assessments that are subject to bias and symptomatic reporting that rely on compliance. An objective and easily obtained biomarker that can indicate recovery following SRC would aid clinicians to make safer RTP decisions. We performed a systematic review to identify potential biomarkers from saliva, urine and blood sources that could inform the clinical RTP decision. The MEDLINE database was searched. Inclusion criteria were studies focusing on adults diagnosed with SRC, fluid biomarkers from blood, saliva or urine and clinical recovery from SRC or at RTP. We assessed each biomarker for their time course post SRC and relationship to clinical recovery. Secondary outcomes included correlation with symptom scores and predictive value for prolonged RTP. We identified 8 studies all investigating blood-based markers of diffuse axonal injury (tau, NFL, SNTF), neuroglial injury (NSE, VLP-1, UCH-L1, S100B, GFAP), inflammation and hormonal disturbances. Tau, SNTF, UCH-1, GFAP, S100B and the inflammatory cytokine MCP-4 are raised post SRC and return to baseline by RTP. Changes in tau, NFL, SNTF, GFAP and MCP-4 post SRC correlate with severity of concussion as measured by symptom severity or RTP duration. There is only preliminary case-reporting for hormonal biomarkers. The evidence is limited by a lack of highly powered studies, variation in use of athletic and Contact sport controls (CSC) and a lack of consistent sampling and assessment protocols. There is promise for biomarkers to aid RTP decisions following SRC, most notably in use alongside clinical assessment in RTP criteria to allow greater precision in identifying mild and severe concussion.
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Yue, John K., Pavan S. Upadhyayula, Lauro N. Avalos, Hansen Deng, and Kevin K. W. Wang. "The Role of Blood Biomarkers for Magnetic Resonance Imaging Diagnosis of Traumatic Brain Injury." Medicina 56, no. 2 (February 22, 2020): 87. http://dx.doi.org/10.3390/medicina56020087.
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Background and Objectives: The annual global incidence of traumatic brain injury (TBI) is over 10 million. An estimated 29% of TBI patients with negative computed tomography (CT−) have positive magnetic resonance imaging (MRI+) findings. Judicious use of serum biomarkers with MRI may aid in diagnosis of CT-occult TBI. The current manuscript aimed to evaluate the diagnostic, therapeutic and risk-stratification utility of known biomarkers and intracranial MRI pathology. Materials and Methods: The PubMed database was queried with keywords (plasma OR serum) AND (biomarker OR marker OR protein) AND (brain injury/trauma OR head injury/trauma OR concussion) AND (magnetic resonance imaging/MRI) (title/abstract) in English. Seventeen articles on TBI biomarkers and MRI were included: S100 calcium-binding protein B (S100B; N = 6), glial fibrillary acidic protein (GFAP; N = 3), GFAP/ubiquitin carboxyl-terminal hydrolase-L1 (UCH-L1; N = 2), Tau (N = 2), neurofilament-light (NF-L; N = 2), alpha-synuclein (N = 1), and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor peptide (AMPAR; N = 1). Results: Acute GFAP distinguished CT−/MRI+ from CT−/MRI− (AUC = 0.777, 0.852 at 9–16 h). GFAP discriminated CT−/diffuse axonal injury (DAI+) from controls (AUC = 0.903). Tau correlated directly with number of head strikes and inversely with white matter fractional anisotropy (FA), and a cutoff > 1.5 pg/mL discriminated between DAI+ and DAI− (sensitivity = 74%/specificity = 69%). NF-L had 100% discrimination of DAI in severe TBI and correlated with FA. Low alpha-synuclein was associated with poorer functional connectivity. AMPAR cutoff > 0.4 ng/mL had a sensitivity of 91% and a specificity of 92% for concussion and was associated with minor MRI findings. Low/undetectable S100B had a high negative predictive value for CT/MRI pathology. UCH-L1 showed no notable correlations with MRI. Conclusions: An acute circulating biomarker capable of discriminating intracranial MRI abnormalities is critical to establishing diagnosis for CT-occult TBI and can triage patients who may benefit from outpatient MRI, surveillance and/or follow up with TBI specialists. GFAP has shown diagnostic potential for MRI findings such as DAI and awaits further validation. Tau shows promise in detecting DAI and disrupted functional connectivity. Candidate biomarkers should be evaluated within the context of analytical performance of the assays used, as well as the post-injury timeframe for blood collection relative to MRI abnormalities.
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Al-Enezi, Eiman, Alexandre Vakurov, Amy Eades, Mingyu Ding, Gin Jose, Sikha Saha, and Paul Millner. "Affimer-Based Europium Chelates Allow Sensitive Optical Biosensing in a Range of Human Disease Biomarkers." Sensors 21, no. 3 (January 27, 2021): 831. http://dx.doi.org/10.3390/s21030831.
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The protein biomarker measurement has been well-established using ELISA (enzyme-linked immunosorbent assay), which offers good sensitivity and specificity, but remains slow and expensive. Certain clinical conditions, where rapid measurement or immediate confirmation of a biomarker is paramount for treatment, necessitate more rapid analysis. Biosensors offer the prospect of reagent-less, processing-free measurements at the patient’s bedside. Here, we report a platform for biosensing based on chelated Eu3+ against a range of proteins including biomarkers of cardiac injury (human myoglobin), stroke (glial fibrillary acidic protein (GFAP)), inflammation (C-reactive protein (CRP)) and colorectal cancer (carcinoembryonic antigen (CEA)). The Eu3+ ions are chelated by modified synthetic binding proteins (Affimers), which offer an alternative targeting strategy to existing antibodies. The fluorescence characteristics of the Eu3+ complex with modified Affimers against human myoglobin, GFAP, CRP and CEA were measured in human serum using λex = 395 nm, λem = 590 and 615 nm. The Eu3+-Affimer based complex allowed sensitive detection of human myoglobin, GFAP, CRP and CEA proteins as low as 100 fM in (100-fold) diluted human serum samples. The unique dependence on Eu3+ fluorescence in the visible region (590 and 615 nm) was exploited in this study to allow rapid measurement of the analyte concentration, with measurements in 2 to 3 min. These data demonstrate that the Affimer based Eu3+ complexes can function as nanobiosensors with potential analytical and diagnostic applications.
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Halbgebauer, Rebecca, Steffen Halbgebauer, Patrick Oeckl, Petra Steinacker, Eberhard Weihe, Martin K. H. Schafer, Francesco Roselli, Florian Gebhard, Markus Huber-Lang, and Markus Otto. "Neurochemical Monitoring of Traumatic Brain Injury by the Combined Analysis of Plasma Beta-Synuclein, NfL, and GFAP in Polytraumatized Patients." International Journal of Molecular Sciences 23, no. 17 (August 25, 2022): 9639. http://dx.doi.org/10.3390/ijms23179639.
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Traumatic brain injury (TBI) represents a major determining factor of outcome in severely injured patients. However, reliable brain-damage-monitoring markers are still missing. We therefore assessed brain-specific beta-synuclein as a novel blood biomarker of synaptic damage and measured the benchmarks neurofilament light chain (NfL), as a neuroaxonal injury marker, and glial fibrillary acidic protein (GFAP), as an astroglial injury marker, in patients after polytrauma with and without TBI. Compared to healthy volunteers, plasma NfL, beta-synuclein, and GFAP were significantly increased after polytrauma. The markers demonstrated highly distinct time courses, with beta-synuclein and GFAP peaking early and NfL concentrations gradually elevating during the 10-day observation period. Correlation analyses revealed a distinct influence of the extent of extracranial hemorrhage and the severity of head injury on biomarker concentrations. A combined analysis of beta-synuclein and GFAP effectively discriminated between polytrauma patients with and without TBI, despite the comparable severity of injury. Furthermore, we found a good predictive performance for fatal outcome by employing the initial plasma concentrations of NfL, beta-synuclein, and GFAP. Our findings suggest a high diagnostic value of neuronal injury markers reflecting distinct aspects of neuronal injury for the diagnosis of TBI in the complex setting of polytrauma, especially in clinical surroundings with limited imaging opportunities.
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Krausz, Alyse D., Frederick K. Korley, and Mark A. Burns. "A Variable Height Microfluidic Device for Multiplexed Immunoassay Analysis of Traumatic Brain Injury Biomarkers." Biosensors 11, no. 9 (September 7, 2021): 320. http://dx.doi.org/10.3390/bios11090320.
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Traumatic brain injury (TBI) is a leading cause of global morbidity and mortality, partially due to the lack of sensitive diagnostic methods and efficacious therapies. Panels of protein biomarkers have been proposed as a way of diagnosing and monitoring TBI. To measure multiple TBI biomarkers simultaneously, we present a variable height microfluidic device consisting of a single channel that varies in height between the inlet and outlet and can passively multiplex bead-based immunoassays by trapping assay beads at the point where their diameter matches the channel height. We developed bead-based quantum dot-linked immunosorbent assays (QLISAs) for interleukin-6 (IL-6), glial fibrillary acidic protein (GFAP), and interleukin-8 (IL-8) using DynabeadsTM M-450, M-270, and MyOneTM, respectively. The IL-6 and GFAP QLISAs were successfully multiplexed using a variable height channel that ranged in height from ~7.6 µm at the inlet to ~2.1 µm at the outlet. The IL-6, GFAP, and IL-8 QLISAs were also multiplexed using a channel that ranged in height from ~6.3 µm at the inlet to ~0.9 µm at the outlet. Our system can keep pace with TBI biomarker discovery and validation, as additional protein biomarkers can be multiplexed simply by adding in antibody-conjugated beads of different diameters.
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Husain, H., W. Savage, A. Everett, X. Ye, C. Blair, K. E. Romans, C. Bettegowda, P. Burger, S. A. Grossman, and M. Holdhoff. "The role of plasma GFAP as a biomarker for glioblastoma." Journal of Clinical Oncology 29, no. 15_suppl (May 20, 2011): 2095. http://dx.doi.org/10.1200/jco.2011.29.15_suppl.2095.
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Kim, Hyunjin, Eun-Jae Lee, Seungmi Kim, Lyn-Kyung Choi, Keonwoo Kim, Hye Weon Kim, Kwang-Kuk Kim, and Young-Min Lim. "Serum biomarkers in myelin oligodendrocyte glycoprotein antibody–associated disease." Neurology - Neuroimmunology Neuroinflammation 7, no. 3 (March 17, 2020): e708. http://dx.doi.org/10.1212/nxi.0000000000000708.
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ObjectiveTo test the hypothesis that the pattern of serum biomarkers of disease activity and disability in myelin oligodendrocyte glycoprotein antibody–associated disease (MOGAD) will be different from those in neuromyelitis optica spectrum disorder (NMOSD) with anti–aquaporin-4 antibodies (AQP4-Abs).MethodsUsing ultrasensitive single-molecule array assays, we measured neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), and tau in the sera of consecutive patients with MOGAD (n = 16) and NMOSD with AQP4-Ab (n = 33). Serum biomarker levels were compared between patients in relapse and remission states, and correlations between the levels of these biomarkers and Expanded Disability Status Scale (EDSS) scores were analyzed within each group.ResultsIn the MOGAD group, the serum tau level was higher in a relapse state than in a remission state (relapse vs remission: 0.5 [0.4–0.5] vs 0.2 [0.1–0.3] pg/mL, p = 0.027). Both serum levels of NfL and tau correlated with the EDSS score (NfL: r = 0.684, p = 0.003; tau: r = 0.524, p = 0.045). Meanwhile, in the NMOSD group, serum NfL and GFAP levels were higher in a relapse state than in a remission state (relapse vs remission: NfL, 34.8 [12.2–62.3] vs 13.0 [11.3–20.0] pg/mL, p = 0.010; GFAP, 253.8 [150.6–303.0] vs 104.4 [93.9–127.9] pg/mL, p = 0.016). Only the serum GFAP level correlated with the EDSS score (r = 0.485, p = 0.012).ConclusionThe pattern of serum biomarkers of disease activity and disability in MOGAD showed a distinct feature from those in NMOSD with AQP4-Ab, which implicates different pathogeneses between the 2 diseases.
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Heller, Carolin, Martha S. Foiani, Katrina Moore, Rhian Convery, Martina Bocchetta, Mollie Neason, David M. Cash, et al. "Plasma glial fibrillary acidic protein is raised in progranulin-associated frontotemporal dementia." Journal of Neurology, Neurosurgery & Psychiatry 91, no. 3 (January 14, 2020): 263–70. http://dx.doi.org/10.1136/jnnp-2019-321954.
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BackgroundThere are few validated fluid biomarkers in frontotemporal dementia (FTD). Glial fibrillary acidic protein (GFAP) is a measure of astrogliosis, a known pathological process of FTD, but has yet to be explored as potential biomarker.MethodsPlasma GFAP and neurofilament light chain (NfL) concentration were measured in 469 individuals enrolled in the Genetic FTD Initiative: 114 C9orf72 expansion carriers (74 presymptomatic, 40 symptomatic), 119 GRN mutation carriers (88 presymptomatic, 31 symptomatic), 53 MAPT mutation carriers (34 presymptomatic, 19 symptomatic) and 183 non-carrier controls. Biomarker measures were compared between groups using linear regression models adjusted for age and sex with family membership included as random effect. Participants underwent standardised clinical assessments including the Mini-Mental State Examination (MMSE), Frontotemporal Lobar Degeneration-Clinical Dementia Rating scale and MRI. Spearman’s correlation coefficient was used to investigate the relationship of plasma GFAP to clinical and imaging measures.ResultsPlasma GFAP concentration was significantly increased in symptomatic GRN mutation carriers (adjusted mean difference from controls 192.3 pg/mL, 95% CI 126.5 to 445.6), but not in those with C9orf72 expansions (9.0, –61.3 to 54.6), MAPT mutations (12.7, –33.3 to 90.4) or the presymptomatic groups. GFAP concentration was significantly positively correlated with age in both controls and the majority of the disease groups, as well as with NfL concentration. In the presymptomatic period, higher GFAP concentrations were correlated with a lower cognitive score (MMSE) and lower brain volume, while in the symptomatic period, higher concentrations were associated with faster rates of atrophy in the temporal lobe.ConclusionsRaised GFAP concentrations appear to be unique to GRN-related FTD, with levels potentially increasing just prior to symptom onset, suggesting that GFAP may be an important marker of proximity to onset, and helpful for forthcoming therapeutic prevention trials.
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Thebault, S., H. Lee, D. Tessier, M. Bowman, A. Bar-Or, D. Arnold, H. Atkins, and M. Freedman. "A.02 Serum biomarkers of MS disease activity in patients treated with bone marrow transplant." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 46, s1 (June 2019): S8. http://dx.doi.org/10.1017/cjn.2019.84.
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Background: There is an unmet need for blood-based biomarkers that can reliably detect MS disease activity. Serum Biomarkers of interest includ Neurofilament-light-chain (NfL), Glial-fibrillary-strocyte-protein(GFAP) and Tau. Bone Marrow Transplantation (BMT) is reserved for aggressive forms of MS and has been shown to halt detectable CNS inflammatory activity for prolonged periods. Significant pre-treatment tissue damage at followed by inflammatory disease abeyance should be reflected longitudinal sera collected from these patients. Methods: Sera were collected from 23 MS patients pre-treatment, and following BMT at 3, 6, 9 and 12-months in addition from 33 non-inflammatory neurological controls. Biomarker quantification was performed with SiMoA. Results: Pre-AHSCT levels of serum NfL and GFAP but not Tau were elevated compared to controls (p=0.0001), and NfL correlated with lesion-based disease activity (6-month-relapse, MRI-T2 and Gadolinium-enhancement). 3-months post-treatment, while NfL levels remained elevated, Tau/GFAP paradoxically increased (p=0.0023/0.0017). These increases at 3m correlated with MRI ‘pseudoatrophy’ at 6-months. NfL/Tau levels dropped to that of controls by 6-months (p=0.0036/0.0159). GFAP levels dropped progressively after 6-months although even at 12-months remained higher than controls (p=0.004). Conclusions: NfL was the closest correlate of MS disease activity and treatment response. Chemotherapy-related toxicity may account for transient increases in NfL, Tau and MRI brain atrophy post-BMT.
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Celikbilek, Asuman, Mehmet Celikbilek, Seda Sabah, Nermin Tanık, Elif Borekci, Serkan Dogan, Yavuz Akin, et al. "The Serum S100B Level as a Biomarker of Enteroglial Activation in Patients with Ulcerative Colitis." International Journal of Inflammation 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/986525.
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Objective. Recent studies have demonstrated that enteric glial cells (EGC) participate in the homeostasis of the gastrointestinal tract. This study investigated whether enteroglial markers, including S100B protein and glial fibrillary acidic protein (GFAP), can serve as noninvasive indicators of EGC activation and disease activity in UC patients.Methods. This clinical prospective study included 35 patients with UC and 40 age- and sex-matched controls. The diagnosis of UC was based on standard clinical, radiological, endoscopic, and histological criteria. Clinical disease activity was evaluated using the Modified Truelove-Witts Severity Index. Serum samples were analyzed for human GFAP and S100B using commercial enzyme-linked immunosorbent assay kits.Results. GFAP was not detected in the serum of either UC patients or controls (P>0.05). However, we found a significant (P<0.001) decrease in the serum S100B levels in the UC patients. No correlation between the serum S100B level and the disease activity or duration was observed (P>0.05). The serum S100B levels did not differ between UC patients with active disease (24 patients, 68.6%) or in remission (11 patients, 31.4%) (P>0.05).Conclusions. Ulcerative colitis patients had significantly lower serum S100B levels, while GFAP was of no diagnostic value in UC patients.
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Benussi, Alberto, Nicholas J. Ashton, Thomas K. Karikari, Stefano Gazzina, Enrico Premi, Luisa Benussi, Roberta Ghidoni, et al. "Serum Glial Fibrillary Acidic Protein (GFAP) Is a Marker of Disease Severity in Frontotemporal Lobar Degeneration." Journal of Alzheimer's Disease 77, no. 3 (September 29, 2020): 1129–41. http://dx.doi.org/10.3233/jad-200608.
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Background: It is still unknown if serum glial fibrillary acidic protein (GFAP) is a useful marker in frontotemporal lobar degeneration (FTLD). Objective: To assess the diagnostic and prognostic value of serum GFAP in a large cohort of patients with FTLD. Methods: In this retrospective study, performed on 406 participants, we measured serum GFAP concentration with an ultrasensitive Single molecule array (Simoa) method in patients with FTLD, Alzheimer’s disease (AD), and in cognitively unimpaired elderly controls. We assessed the role of GFAP as marker of disease severity by analyzing the correlation with clinical variables, neurophysiological data, and cross-sectional brain imaging. Moreover, we evaluated the role of serum GFAP as a prognostic marker of disease survival. Results: We observed significantly higher levels of serum GFAP in patients with FTLD syndromes, except progressive supranuclear palsy, compared with healthy controls, but not compared with AD patients. In FTLD, serum GFAP levels correlated with measures of cognitive dysfunction and disease severity, and were associated with indirect measures of GABAergic deficit. Serum GFAP concentration was not a significant predictor of survival. Conclusion: Serum GFAP is increased in FTLD, correlates with cognition and GABAergic deficits, and thus shows promise as a biomarker of disease severity in FTLD.
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Giovannoni, Gavin. "Multiple Sclerosis Cerebrospinal Fluid Biomarkers." Disease Markers 22, no. 4 (2006): 187–96. http://dx.doi.org/10.1155/2006/509476.
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Cerebrospinal fluid (CSF) is the body fluid closest to the pathology of multiple sclerosis (MS). For many candidate biomarkers CSF is the only fluid that can be investigated. Several factors need to be standardized when sampling CSF for biomarker research: time/volume of CSF collection, sample processing/storage, and the temporal relationship of sampling to clinical or MRI markers of disease activity. Assays used for biomarker detection must be validated so as to optimize the power of the studies. A formal method for establishing whether or not a particular biomarker can be used as a surrogate end-point needs to be adopted. This process is similar to that used in clinical trials, where the reporting of studies has to be done in a standardized way with sufficient detail to permit a critical review of the study and to enable others to reproduce the study design. A commitment must be made to report negative studies so as to prevent publication bias. Pre-defined consensus criteria need to be developed for MS-related prognostic biomarkers. Currently no candidate biomarker is suitable as a surrogate end-point. Bulk biomarkers of the neurodegenerative process such as glial fibrillary acidic protein (GFAP) and neurofilaments (NF) have advantages over intermittent inflammatory markers.
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Papa, Linda, Mark R. Zonfrillo, Robert D. Welch, Lawrence M. Lewis, Carolina F. Braga, Ciara N. Tan, Neema J. Ameli, et al. "Evaluating glial and neuronal blood biomarkers GFAP and UCH-L1 as gradients of brain injury in concussive, subconcussive and non-concussive trauma: a prospective cohort study." BMJ Paediatrics Open 3, no. 1 (August 2019): e000473. http://dx.doi.org/10.1136/bmjpo-2019-000473.
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ObjectivesTo evaluate the ability of glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase (UCH-L1) to detect concussion in children and adult trauma patients with a normal mental status and assess biomarker concentrations over time as gradients of injury in concussive and non-concussive head and body trauma.DesignLarge prospective cohort study.SettingThree level I trauma centres in the USA.ParticipantsPaediatric and adult trauma patients of all ages, with and without head trauma, presenting with a normal mental status (Glasgow Coma Scale score of 15) within 4 hours of injury. Rigorous screening for concussive symptoms was conducted. Of 3462 trauma patients screened, 751 were enrolled and 712 had biomarker data. Repeated blood sampling was conducted at 4, 8, 12, 16, 24, 36, 48, 60, 72, 84, 96, 108, 120, 132, 144, 156, 168 and 180 hours postinjury in adults.Main outcomesDetection of concussion and gradients of injury in children versus adults by comparing three groups of patients: (1) those with concussion; (2) those with head trauma without overt signs of concussion (non-concussive head trauma controls) and (3) those with peripheral (body) trauma without head trauma or concussion (non-concussive body trauma controls).ResultsA total of 1904 samples from 712 trauma patients were analysed. Within 4 hours of injury, there were incremental increases in levels of both GFAP and UCH-L1 from non-concussive body trauma (lowest), to mild elevations in non-concussive head trauma, to highest levels in patients with concussion. In concussion patients, GFAP concentrations were significantly higher compared with body trauma controls (p<0.001) and with head trauma controls (p<0.001) in both children and adults, after controlling for multiple comparisons. However, for UCH-L1, there were no significant differences between concussion patients and head trauma controls (p=0.894) and between body trauma and head trauma controls in children. The AUC for initial GFAP levels to detect concussion was 0.80 (0.73–0.87) in children and 0.76 (0.71–0.80) in adults. This differed significantly from UCH-L1 with AUCs of 0.62 (0.53–0.72) in children and 0.69 (0.64–0.74) in adults.ConclusionsIn a cohort of trauma patients with normal mental status, GFAP outperformed UCH-L1 in detecting concussion in both children and adults. Blood levels of GFAP and UCH-L1 showed incremental elevations across three injury groups: from non-concussive body trauma, to non-concussive head trauma, to concussion. However, UCH-L1 was expressed at much higher levels than GFAP in those with non-concussive trauma, particularly in children. Elevations in both biomarkers in patients with non-concussive head trauma may be reflective of a subconcussive brain injury. This will require further study.
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Amalia, Lisda. "Glial Fibrillary Acidic Protein (GFAP): Neuroinflammation Biomarker in Acute Ischemic Stroke." Journal of Inflammation Research Volume 14 (December 2021): 7501–6. http://dx.doi.org/10.2147/jir.s342097.
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Hansen, Niels, Carolin Rauter, and Jens Wiltfang. "Blutbasierte Biomarker zur Optimierung der Früh- und Differentialdiagnostik der Alzheimer-Demenz." Fortschritte der Neurologie · Psychiatrie 90, no. 07/08 (July 2022): 326–35. http://dx.doi.org/10.1055/a-1839-6237.
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Zusammenfassung Ziele der Studie Die Demenz bei Alzheimer-Krankheit ist eine globale Herausforderung. Studien weisen auf Blutbiomarker zur Diagnose der Alzheimer-Krankheit als eine minimal invasive, schnellere, kostengünstigere und daher zukunftsträchtige Methode hin. Ziel dieser Übersicht ist es, Studien zu vielversprechenden Biomarkern der Alzheimer-Krankheit darzustellen. Methodik Für diese Übersichtsarbeit wurden aktuelle Studien zusammengestellt. Ergebnisse Immunassays mit anschließender Massenspektrometrie und solche mit immunmagnetischer Reduktion sind aussichtsreiche Methoden für die Bestimmung von Amyloid-ß 42 (Aß42) und Amyloid-ß 40 (Aß40) für die Bildung der Ratio von Aß42/Aß40 zur blutbasierten Früh- und Differentialdiagnostik der Alzheimer-Krankheit. Die Amyloid-ß (Aß) Peptide im Blutplasma sind ein potentieller Marker der Aß-Pathologie, da sie mit der Aß-Pathologie im Gehirn korrelieren. Das mittels der Simoa Technologie bestimmte phosphorylierte Tau-Protein 181 (p-tau181), das phosphorylierte Tau Protein 231 (p-tau231) und das phosphorylierte Tau Protein 217 (p-tau217) im Blut sind vielversprechend hinsichtlich einer möglichen Optimierung der Früh- und Differentialdiagnostik der Alzheimer-Krankheit und sind Marker einer Tau-Pathologie im Gehirn. Die Neurofilamente Leichtketten (Nfl) und das saure Gliafaserprotein (GFAP) sind als Zusatzmarker hilfreich, um eine axonale und astrogliale Hirnschädigung bei Alzheimer-Krankheit zu beurteilen. GFAP im Blut könnte vor allem als Zusatzmarker zur Frühdiagnostik und Prädiktion des Verlaufs der Alzheimer-Krankheit sinnvoll sein. Schlussfolgerungen Blutbasierte Biomarker sind ein wichtiger Schritt in Richtung einer weniger invasiven und kostengünstigeren Diagnostik der Alzheimer-Krankheit. Die Ratio Aß42/Aß40, das p-tau181, das p-tau217, das p-tau231, die Nfl und das GFAP sind vielversprechende Blutbiomarker unter Beachtung der AT(N) Klassifikation der Alzheimer-Krankheit. Hochdurchsatzfähige Methoden sollten in großen Kohorten und Metanalysen evaluiert werden. Zudem sollten Konsensus Kriterien mit einheitlichen Protokollen mit Normwerten zur Messung dieser Biomarker erstellt werden. Die Etablierung der AT(N) Klassifikation der Alzheimer-Krankheit im Blut ist unter Berücksichtigung ethischer Gesichtspunkte sowie des Alzheimer Phänotyps ein wichtiger Baustein für die Implementierung einer minimal-invasiven Präzisionsmedizin.
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Luger, Sebastian, Jens Witsch, Andreas Dietz, Gerhard F. Hamann, Jens Minnerup, Hauke Schneider, Matthias Sitzer, Katja E. Wartenberg, Marion Niessner, and Christian Foerch. "Glial Fibrillary Acidic Protein Serum Levels Distinguish between Intracerebral Hemorrhage and Cerebral Ischemia in the Early Phase of Stroke." Clinical Chemistry 63, no. 1 (January 1, 2017): 377–85. http://dx.doi.org/10.1373/clinchem.2016.263335.
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Abstract BACKGROUND Recent studies have suggested that glial fibrillary acidic protein (GFAP) serum concentrations distinguish between intracerebral hemorrhage (ICH) and ischemic stroke (IS) shortly after symptom onset. In this prospective multicenter trial we validated GFAP in an independent patient cohort and assessed the quantitative relationship between GFAP release, bleeding size, and localization. METHODS We included patients with a persistent neurological deficit (NIH Stroke Scale ≥4) suggestive of stroke within 6 h of symptom onset. Blood samples were drawn at hospital admission. GFAP serum concentrations were measured using an electrochemiluminometric immunoassay. Primary endpoint was the final diagnosis established at hospital discharge (ICH, IS, or stroke mimic). RESULTS 202 patients were included (45 with ICH, 146 with IS, 11 stroke mimics). GFAP concentrations were significantly higher in ICH than in IS patients [median (interquartile range) 0.16 μg/L (0.04–3.27) vs 0.01 μg/L (0.01–0.01), P <0.001]. A GFAP cutoff of 0.03 μg/L provided a sensitivity of 77.8% and a specificity of 94.2% in distinguishing ICH from IS and stroke mimics [ROC analysis area under the curve 0.872 (95% CI, 0.802–0.942), P <0.001]. GFAP serum concentrations were positively correlated with ICH volume. Lobar ICH volumes were larger and thus associated with higher GFAP concentrations as compared to deep ICH. CONCLUSIONS Serum GFAP was confirmed to be a biomarker indicating ICH in patients presenting with acute stroke symptoms. Very small ICH may be missed owing to less tissue destruction.
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Liu, Lili, Hua Zhu, Yanchun Yan, Peng Lv, and Wei Wu. "Toxicity Evaluation and Biomarker Selection with Validated Reference Gene in Embryonic Zebrafish Exposed to Mitoxantrone." International Journal of Molecular Sciences 19, no. 11 (November 8, 2018): 3516. http://dx.doi.org/10.3390/ijms19113516.
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Notwithstanding the widespread use and promising clinical value of chemotherapy, the pharmacokinetics, toxicology, and mechanism of mitoxantrone remains unclear. To promote the clinical value in the treatment of human diseases and the exploration of potential subtle effects of mitoxantrone, zebrafish embryos were employed to evaluate toxicity with validated reference genes based on independent stability evaluation programs. The most stable and recommended reference gene was gapdh, followed by tubα1b, for the 48 h post fertilization (hpf) zebrafish embryo mitoxantrone test, while both eef1a1l1 and rpl13α were recommended as reference genes for the 96 hpf zebrafish embryo mitoxantrone test. With gapdh as an internal control, we analyzed the mRNA levels of representative hepatotoxicity biomarkers, including fabp10a, gclc, gsr, nqo1, cardiotoxicity biomarker erg, and neurotoxicity biomarker gfap in the 48 hpf embryo mitoxantrone test. The mRNA levels of gclc, gsr, and gfap increased significantly in 10 and 50 μg/L mitoxantrone-treated 48 hpf embryos, while the transcript levels of fabp10a decreased in a dose-dependent manner, indicating that mitoxantrone induced hepatotoxicity and neurotoxicity. Liver hematoxylin–eosin staining and the spontaneous movement of embryos confirmed the results. Thus, the present research suggests that mitoxantrone induces toxicity during the development of the liver and nervous system in zebrafish embryos and that fabp10a is recommended as a potential biomarker for hepatotoxicity in zebrafish embryos. Additionally, gapdh is proposed as a reference gene for the 48 hpf zebrafish embryo mitoxantrone toxicity test, while eef1a1l1 and rpl13α are proposed as that for the 96 hpf test.
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Cabezas, Juan Antonio, Alejandro Bustamante, Nicola Giannini, Emilio Pecharroman, Aristeidis H. Katsanos, Georgios Tsivgoulis, Michal Rozanski, et al. "Discriminative value of glial fibrillar acidic protein (GFAP) as a diagnostic tool in acute stroke. Individual patient data meta-analysis." Journal of Investigative Medicine 68, no. 8 (September 8, 2020): 1379–85. http://dx.doi.org/10.1136/jim-2020-001432.
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Glial fibrillar acidic protein (GFAP) in serum has been evaluated as a promising biomarker to differentiate between intracerebral hemorrhage (ICH) and acute ischemic stroke (AIS). We assessed its value as diagnostic and prognostic tool for ICH through a literature systematic review and individual patient data (IPD) meta-analysis.We performed a systematic search in PubMed database until November 2018 for publications that evaluated GFAP to differentiate AIS and ICH within 4.5 hours after symptoms onset. Thereafter, we invited authors of selected studies to participate in this work by providing IPD from their cohorts. We used standardized individual subject’s data to evaluate the association of GFAP concentrations with stroke subtype, demographics, stroke characteristics and factors related with GFAP measurement.From 4 selected studies, we collected data of 340 patients (236 AIS and 104 ICH). Standardized GFAP blood levels were significantly elevated in ICH compared with those with AIS (median and IQR: 0.84 (0.781–1.24), 0.79 (0.74–0.81); p<0.0001). In both stroke types, GFAP concentrations correlated with baseline stroke severity (r=0.27, p<0.0001; r=0.36, p<0.001; for AIS and ICH, respectively) but no correlation was found regarding time to sampling. Limited data precluded the evaluation of GFAP levels and functional outcome.These findings demonstrate substantially different levels of GFAP in the blood of patients with ICH compared with patients with AIS soon after the event, while no association was found with outcome. In summary, GFAP could be a valuable diagnostic tool to assist in medical decision-making and to optimize management of stroke in the acute setting.
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Natarajan, Satheesh, and Jayaraj Joseph. "A novel time-resolved fluorescent lateral flow immunoassay for quantitative detection of the trauma brain injury biomarker-glial fibrillary acidic protein." Sensors & Diagnostics 1, no. 1 (2022): 193–97. http://dx.doi.org/10.1039/d1sd00021g.
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A highly sensitive time-resolved fluorescence lateral flow immunoassay (TRF-LFIA) was developed to quantify glial fibrillary acidic protein (GFAP), a trauma brain injury (TBI) biomarker in blood, for the purpose of providing a diagnosis of mild brain injury.
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Liu, G., and J. Geng. "Glial fibrillary acidic protein as a prognostic marker of acute ischemic stroke." Human & Experimental Toxicology 37, no. 10 (January 8, 2018): 1048–53. http://dx.doi.org/10.1177/0960327117751236.
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Background: We investigated the association between serum levels of glial fibrillary acidic protein (GFAP) and stroke functional outcomes in a cohort of 286 patients with acute ischemic stroke (AIS). Methods: We prospectively studied 286 patients with AIS who were admitted within 24 h after the onset of symptoms. Serum levels of GFAP and National Institutes of Health Stroke Scale (NIHSS) were measured at admission. The primary end point was stroke functional outcome among 1-year after stroke onset. We used logistic regression models to assess the relationship between GFAP levels and stroke outcomes. Results: The GFAP level was obtained with a median value of 0.18 (interquartile ranges (IQRs): 0.09–0.28) ng/ml. In multivariable models adjusted for age, gender, and other risk factors, GFAP levels were associated with an increased risk of a NIHSS>6 (odds ratio (OR) = 1.55; 95% confidence interval (CI): 1.16–1.89; p = 0.012). The poor outcome distribution across the GFAP quartiles ranged between 12.7% (first quartile) and 70.4% (fourth quartile). After adjusting for other established risk factors, in multivariate models comparing the Q3 and Q 4 quartiles against the Q1 of the GFAP, the levels of GFAP were associated with poor outcome, and the adjusted risk of poor outcome increased by 211% (3.11[1.80–5.05], p < 0.001) and 522% (6.22[2.98–11.83], p < 0.001), respectively. Interestingly, GFAP improved the ability of NIHSS score to diagnose poor outcomes (area under the curve [AUC] of the combined model 0.82; 95% CI: 0.77–0.88; p = 0.02). Conclusion: GFAP levels are a novel and complementary biomarker to predict functional outcome 1 year after AIS
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Rhine, Tara, Ting Sa, Nanhua Zhang, Shari Wade, and Rachel P. Berger. "2443." Journal of Clinical and Translational Science 1, S1 (September 2017): 78. http://dx.doi.org/10.1017/cts.2017.276.
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OBJECTIVES/SPECIFIC AIMS: Analyze data from the first 30 children enrolled in a prospective cohort study evaluating the ability of specific serum biomarkers to distinguish children with traumatic brain injuries (TBI) from children with orthopedic injuries (OI). METHODS/STUDY POPULATION: Children ages 0<5 years were eligible if they presented to the emergency department within 6 hours of injury. Children were identified as having a TBI if they sustained a head injury and were found to have an acute injury on head CT. Children were identified as having an OI if they sustained a musculoskeletal injury significant enough to necessitate radiography per clinical care. Individual (eg, age) and clinical (eg, radiography findings) factors, as well as serum biomarkers [eg, ubiquitin C-terminal hydrolase L1 (UCH-L1), glial fibrillary acidic protein (GFAP)] were collected at time of enrollment. TBI and OI groups were compared using Wilcoxon rank-sum and Kruskal-Wallis tests. RESULTS/ANTICIPATED RESULTS: This cohort consisted of 13 children with TBI (7 with isolated skull fractures, 1 with intracranial injury, and 5 with both a skull fracture and an intracranial injury) and 17 with OI (12 with fractures). Most patients were male (67%) and White (67%), and this did not differ between groups (p>0.1). Children with TBI were significantly younger than children with OI, with an average (±standard deviation) age of 15±13 and 39±13 months, respectively (p<0.01). There was not a significant difference in time from injury to biomarker collection between TBI and OI patients at 4.1±1.8 and 5.8±2.6 hours, respectively (p=0.07). Median (IQR) levels of GFAP were significantly higher (p<0.01) in children with TBI, relative to children with OI: 220 (67–421) pg/mL Versus 37 (25–74) pg/mL, respectively. Median (IQR) levels of UCH-L1 were also significantly higher (p<0.01) in the TBI group, relative to children with OI: 444 (377–449) pg/mL Versus 248 (140–417) pg/mL, respectively. In a subanalysis comparing median biomarker levels across three study groups (ie, TBI with an isolated skull fracture, TBI with an intracranial injury, and OI), group differences remained significant for both biomarkers with TBI patients having higher levels, relative to OI patients, of both GFAP (p<0.01) and UCH-L1 (p=0.02). DISCUSSION/SIGNIFICANCE OF IMPACT: GFAP and UCH-L1 hold promise to improve the diagnosis of TBI in very young children. Identification of a marker of TBI that can be done in the acute care setting would advance the diagnosis of TBI in very young children, a vulnerable population for whom identification of neurological symptoms can be challenging.
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Kumpaitiene, Birute, Milda Svagzdiene, Ingrida Drigotiene, Edmundas Sirvinskas, Ramune Sepetiene, Rolandas Zakelis, and Rimantas Benetis. "Correlation among decreased regional cerebral oxygen saturation, blood levels of brain injury biomarkers, and cognitive disorder." Journal of International Medical Research 46, no. 9 (June 13, 2018): 3621–29. http://dx.doi.org/10.1177/0300060518776545.
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Objective This study was performed to investigate the correlation among decreased regional cerebral oxygen saturation (rSO2), blood levels of brain injury biomarkers, and postoperative cognitive disorder (POCD) after cardiac surgery with cardiopulmonary bypass (CPB). Methods This prospective observational study included 59 patients undergoing coronary artery bypass graft surgery with CPB. All patients underwent neuropsychological tests (Mini Mental State Evaluation, Rey Auditory Verbal Learning Test, digit span test, digit symbol substitution test, and Schulte table) the day before and 10 days after the surgery. The blood levels of two brain injury biomarkers, neuron-specific enolase (NSE) and glial fibrillary acidic protein (GFAP), were measured before and 1 day after the surgery. Results The rSO2 decreased during surgery in 21 (35%) patients. POCD was detected in 22 (37%) patients. After the surgery, no significant changes in the GFAP blood level occurred in any patients. No significant correlations were found among the decreased rSO2, increased NSE blood level, and rate of POCD. Conclusion These results suggest that a decrease in rSO2 during cardiac surgery is not necessarily related to the development of POCD or an increased blood level of the brain injury biomarker NSE.
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Bartl, Michael, Mohammed Dakna, Douglas Galasko, Samantha J. Hutten, Tatiana Foroud, Marian Quan, Kenneth Marek, et al. "Biomarkers of neurodegeneration and glial activation validated in Alzheimer’s disease assessed in longitudinal cerebrospinal fluid samples of Parkinson’s disease." PLOS ONE 16, no. 10 (October 7, 2021): e0257372. http://dx.doi.org/10.1371/journal.pone.0257372.
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Aim Several pathophysiological processes are involved in Parkinson’s disease (PD) and could inform in vivo biomarkers. We assessed an established biomarker panel, validated in Alzheimer’s Disease, in a PD cohort. Methods Longitudinal cerebrospinal fluid (CSF) samples from PPMI (252 PD, 115 healthy controls, HC) were analyzed at six timepoints (baseline, 6, 12, 24, 36, and 48 months follow-up) using Elecsys® electrochemiluminescence immunoassays to quantify neurofilament light chain (NfL), soluble TREM2 receptor (sTREM2), chitinase-3-like protein 1 (YKL40), glial fibrillary acidic protein (GFAP), interleukin-6 (IL-6), S100, and total α-synuclein (αSyn). Results αSyn was significantly lower in PD (mean 103 pg/ml vs. HC: 127 pg/ml, p<0.01; area under the curve [AUC]: 0.64), while all other biomarkers were not significantly different (AUC NfL: 0.49, sTREM2: 0.54, YKL40: 0.57, GFAP: 0.55, IL-6: 0.53, S100: 0.54, p>0.05) and none showed a significant difference longitudinally. We found significantly higher levels of all these markers between PD patients who developed cognitive decline during follow-up, except for αSyn and IL-6. Conclusion Except for αSyn, the additional biomarkers did not differentiate PD and HC, and none showed longitudinal differences, but most markers predict cognitive decline in PD during follow-up.
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Leete, J. J., C. L. Pattinson, V. A. Guedes, C. Lai, C. Devoto, A. van der Merwe, S. Lippa, et al. "1118 Examining the Role of Serum and Exosomal Biomarkers in Symptoms of Fatigue and Daytime Sleepiness Following Traumatic Brain Injury." Sleep 43, Supplement_1 (April 2020): A426. http://dx.doi.org/10.1093/sleep/zsaa056.1113.
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Abstract Introduction Fatigue and daytime sleepiness are two of the most common chronic symptoms reported after traumatic brain injury (TBI). However, there is limited understanding of the pathophysiological mechanisms following TBI that result in these symptoms. Previous research has observed elevations in peripheral blood levels of proteins in TBI patients versus controls, including neurofilament light chain (NFL)—predominantly expressed in long myelinated subcortical axons—and glial fibrillary acidic protein (GFAP)—predominantly expressed in reactive astrocytes responding to central nervous system injuries. This study examines the relationship between serum and exosomal NFL and GFAP, and symptoms of fatigue and daytime sleepiness in TBI patients 1-year after injury. Methods Sixty-seven patients with TBIs ranging from mild to severe were included in this study. Blood samples were collected from all participants 1-year post TBI, with concentrations of GFAP and NFL measured in serum and exosomes using Single Molecule Array technology (Simoa), an ultrasensitive assay. Participants reported fatigue using the Fatigue Severity Scale (FSS), and daytime sleepiness using the Epworth Sleepiness Scale (ESS). Results A linear regression model of fatigue symptoms and exosomal NFL controlling for age revealed that fatigue was negatively associated with exosomal NFL concentrations (β = -.317, p = .041, ηp2 = -.343) and accounted for 20.2% of the change in NFL. Serum NFL concentrations were not associated with fatigue, nor were GFAP serum or exosomes. No significant associations were found between NFL, GFAP, and daytime sleepiness. Conclusion Our findings suggest that exosomal NFL may be related to mechanisms underlying TBI-related fatigue and the potential of NFL as a biomarker of fatigue. To our knowledge, this study is the first to examine the relationship between post-TBI NFL levels and fatigue symptoms. Further investigation into serum and exosome biomarkers of TBI-related fatigue and daytime sleepiness is warranted. Support National Institutes of Health and Center for Neuroscience and Regenerative Medicine
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Foerch, Christian, Marion Niessner, Tobias Back, Michael Bauerle, Gian Marco De Marchis, Andreas Ferbert, Holger Grehl, et al. "Diagnostic Accuracy of Plasma Glial Fibrillary Acidic Protein for Differentiating Intracerebral Hemorrhage and Cerebral Ischemia in Patients with Symptoms of Acute Stroke." Clinical Chemistry 58, no. 1 (January 1, 2012): 237–45. http://dx.doi.org/10.1373/clinchem.2011.172676.
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Abstract BACKGROUND Glial fibrillary acidic protein (GFAP) is a biomarker candidate indicative of intracerebral hemorrhage (ICH) in patients with symptoms of acute stroke. GFAP is released rapidly in the presence of expanding intracerebral bleeding, whereas a more gradual release occurs in ischemic stroke. In this study the diagnostic accuracy of plasma GFAP was determined in a prospective multicenter approach. METHODS Within a 1-year recruitment period, patients suspected of having acute (symptom onset <4.5 h before admission) hemispheric stroke were prospectively included into the study in 14 stroke centers in Germany and Switzerland. A blood sample was collected at admission, and plasma GFAP was measured by use of an electrochemiluminometric immunoassay. The final diagnosis, established at hospital discharge, was classified as ICH, ischemic stroke, or stroke mimic. RESULTS The study included 205 patients (39 ICH, 163 ischemic stroke, 3 stroke mimic). GFAP concentrations were increased in patients with ICH compared with patients with ischemic stroke [median (interquartile range) 1.91 μg/L (0.41–17.66) vs 0.08 μg/L (0.02–0.14), P < 0.001]. Diagnostic accuracy of GFAP for differentiating ICH from ischemic stroke and stroke mimic was high [area under the curve 0.915 (95% CI 0.847–0.982), P < 0.001]. A GFAP cutoff of 0.29 μg/L provided diagnostic sensitivity of 84.2% and diagnostic specificity of 96.3% for differentiating ICH from ischemic stroke and stroke mimic. CONCLUSIONS Plasma GFAP analysis performed within 4.5 h of symptom onset can differentiate ICH and ischemic stroke. Studies are needed to evaluate a GFAP point-of-care system that may help optimize the prehospital triage and management of patients with symptoms of acute stroke.
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Abdelhak, Ahmed, Matteo Foschi, Samir Abu-Rumeileh, John K. Yue, Lucio D’Anna, Andre Huss, Patrick Oeckl, et al. "Blood GFAP as an emerging biomarker in brain and spinal cord disorders." Nature Reviews Neurology 18, no. 3 (February 3, 2022): 158–72. http://dx.doi.org/10.1038/s41582-021-00616-3.
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Yovino, Susannah G., Matthias Holdhoff, William J. Savage, Pratima Dulloor, Stuart A. Grossman, and Allen Everett. "Preliminary results of a biomarker discovery project for treatment-related brain injury (TRBI) in malignant glioma." Journal of Clinical Oncology 30, no. 30_suppl (October 20, 2012): 94. http://dx.doi.org/10.1200/jco.2012.30.30_suppl.94.
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94 Background: Patients with malignant glioma often develop increased enhancement in the tumor bed after chemoradiation (CRT). Current imaging techniques cannot distinguish if these changes are due to recurrent disease or treatment-related brain injury (TRBI). Serum biomarkers could help noninvasively make this distinction. Brain-specific proteins have been used as markers of the severity of other brain injuries including stroke, hypoxia, and traumatic brain injury. We hypothesized that similar changes could be observed following brain CRT and could provide preliminary data supporting biomarker development for TRBI. Methods: Patients receiving concurrent radiation and temozolomide (TMZ) for malignant glioma were eligible. The study was approved by the institutional review board. Informed consent was obtained from all patients. Serum is sampled before CRT, in the last week of CRT, and at 1 month, 6 mos, and 1 year after CRT. Neurologic exams, cognitive testing, and imaging are performed at the same intervals. Serum samples were tested for glial fibrillary acidic protein (GFAP), neurogranin, ICAM-5, B-syn-nuclein, and brain-derived neurotrophic factor (BDNF). Samples were measured in duplicate using an electrochemiluminescent immunoassay. Results: Data are available for the first 7 patients enrolled in this study. All of the tested markers except GFAP were measurable at baseline and all other time points. None of the markers were consistently elevated during the last week of CRT or at any other time point during follow-up. Three patients had resection of suspected recurrent disease. Two had recurrent tumor and 1 had no evidence of disease. No correlation was apparent with the findings at surgery and serum levels of GFAP, neurogranin, ICAM-5, B-synuclein, or BDNF. Conclusions: This study describes a mechanism for identifying a serum protein marker of TRBI. Preliminary results did not identify elevations in any of the selected markers immediately after CRT when signs of TRBI should be apparent or at other points in the clinical course. Testing of additional serum markers is needed to identify a biomarker of TRBI which would provide valuable information for managing high-grade glioma patients.
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González-López, Andrea, Estefanía Costa-Rama, Carmen García-Cabo Fernández, Lorena Benavente-Fernández, Sergio Calleja-Puerta, Beatriz Fernández-García, Rosario Pereiro, and M. Teresa Fernández-Abedul. "Microcentrifuge Tubes as Disposable Immunoelectrochemical Cells for the On-Site Determination of GFAP, Biomarker of Hemorrhagic Stroke." Proceedings 60, no. 1 (November 2, 2020): 10. http://dx.doi.org/10.3390/iecb2020-07060.
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Stroke is the leading cause of mortality worldwide. Differentiating patients with intracerebral hemorrhage (ICH) or ischemic stroke in the first hours of symptoms onset is of paramount importance to the optimal management of patients. Current diagnosis of acute stroke relies on neuroimaging techniques that provide valuable information but not always are readily available. In this context, the development of analytical tools capable of a rapid and on-site differentiation between the types of stroke is an important challenge with great socio-economic benefits. Glial fibrillary acidic protein (GFAP) is considered one of the ICH biomarkers in patients with symptoms of acute stroke. In this work, a simple electroanalytical device for the analysis of GFAP was developed combining stainless-steel pins and a microcentrifuge tube. The sandwich immunoassay for the determination of GFAP was carried out inside the microcentrifuge tube immobilizing the capture antibody on the bottom of the tube. The three stainless-steel pins acting as electrodes were inserted in the cap in such a way that, when the immunoassay is finished, the tube is turned bottom up allowing the electrochemical detection in the same tube.
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Kleerekooper, Iris, Megan K. Herbert, H. Bea Kuiperij, Douglas Kazutoshi Sato, Kazuo Fujihara, Dagoberto Callegaro, Romain Marignier, et al. "CSF levels of glutamine synthetase and GFAP to explore astrocytic damage in seronegative NMOSD." Journal of Neurology, Neurosurgery & Psychiatry 91, no. 6 (March 26, 2020): 605–11. http://dx.doi.org/10.1136/jnnp-2019-322286.
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ObjectiveTo explore levels of astrocytopathy in neuromyelitis optica spectrum disorder (NMOSD) by measuring levels of the astrocytic enzyme glutamine synthetase (GS) and glial fibrillary acidic protein (GFAP), an established astrocytic biomarker known to be associated with disease activity in multiple sclerosis.MethodsCerebrospinal fluid concentrations of GS and GFAP were measured by ELISA in patients with NMOSD (n=39, 28 aquaporin-4 (AQP4)-Ab-seropositive, 3 double-Ab-seronegative, 4 myelin oligodendrocyte glycoprotein (MOG)-Ab-seropositive and 4 AQP4-Ab-seronegative with unknown MOG-Ab-serostatus), multiple sclerosis (MS) (n=69), optic neuritis (n=5) and non-neurological controls (n=37).ResultsGFAP and GS concentrations differed significantly across groups (both p<0.001), showing a similar pattern of elevation in patients with AQP4-Ab-seropositive NMOSD. GS and GFAP were significantly correlated, particularly in patients with AQP4-Ab-seropositive NMOSD (rs=0.70, p<0.001). Interestingly, GFAP levels in some patients with double-Ab-seronegative NMOSD were markedly increased.ConclusionsOur data indicate astrocytic injury occurs in some patients with double-Ab-seronegative NMOSD, which hints at the possible existence of yet undiscovered astrocytic autoimmune targets. We hypothesise that elevated GS and GFAP levels could identify those double-Ab-seronegative patients suitable to undergo in-depth autoimmune screening for astrocytic antibodies.
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Holdhoff, Matthias, Susannah G. Yovino, William J. Savage, Pratima Dulloor, Stuart A. Grossman, and Allen Everett. "Pre- and postoperative plasma concentrations of five novel candidate biomarker proteins in patients with high- and low-grade gliomas." Journal of Clinical Oncology 30, no. 30_suppl (October 20, 2012): 21. http://dx.doi.org/10.1200/jco.2012.30.30_suppl.21.
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21 Background: Current imaging techniques are unable to accurately measure tumor burden in gliomas, because they rely on blood-brain barrier (BBB) permeability that is altered following surgery, radiation, steroids, and antiangiogenic therapies. This often leads to misinterpretation of disease status and incorrect clinical decisions. The development of tumor-specific blood-based markers for gliomas is therefore critically important. This study evaluates the detectability of five novel protein biomarker candidates in the plasma of patients with gliomas: neurogranin, ICAM-5, beta-synuclein, brain-derived neurotrophic factor (BDNF), and glial fibrillary acidic protein (GFAP). These biomarker candidates were chosen because of their specificity for brain tissue. Methods: Pre- and postoperative plasma samples were obtained from patients with newly diagnosed gliomas with IRB approval. Plasma concentrations were measured in duplicates using an electrochemiluminescent immunoassay with a lower limit of quantification of >0.04ng/mL (GFAP) and >0.02 ng/mL (other markers). Results: Plasma levels were detectable for all 5 tested markers at baseline and postoperatively. Baseline levels were highly variable and postoperative GFAP levels were much higher than preoperative levels likely related to brain injury (see table). Conclusions: Five potentially useful protein markers have been identified in the plasma of patients with gliomas. Further studies are underway to assess the specificity of each marker and its ability to detect dynamic changes in tumor burden. [Table: see text]
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Kalra, Love-Preet, Himani Khatter, Sarvotham Ramanathan, Sameer Sapehia, Kavita Devi, Abirami Kaliyaperumal, Deepti Bal, et al. "Serum GFAP for stroke diagnosis in regions with limited access to brain imaging (BE FAST India)." European Stroke Journal 6, no. 2 (May 11, 2021): 176–84. http://dx.doi.org/10.1177/23969873211010069.
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Introduction Despite a high burden of stroke, access to rapid brain imaging is limited in many middle- and low-income countries. Previous studies have described the astroglial protein GFAP (glial fibrillary acidic protein) as a biomarker of intracerebral hemorrhage. The aim of this study was to test the diagnostic accuracy of GFAP for ruling out intracranial hemorrhage in a prospective cohort of Indian stroke patients. Patients and methods This study was conducted in an Indian tertiary hospital (Christian Medical College, Ludhiana). Patients with symptoms suggestive of acute stroke admitted within 12 h of symptom onset were enrolled. Blood samples were collected at hospital admission. Single Molecule Array technology was used for determining serum GFAP concentrations. Results A total number of 155 patients were included (70 intracranial hemorrhage, 75 ischemic stroke, 10 stroke mimics). GFAP serum concentrations were elevated in intracranial hemorrhage patients compared to ischemic stroke patients [median (interquartile range) 2.36 µg/L (0.61–7.16) vs. 0.18 µg/L (0.11–0.38), p < 0.001]. Stroke mimics patients had a median GFAP serum level of 0.14 µg/L (0.09–0.26). GFAP values below the cut-off of 0.33 µg/L (area under the curve 0.871) ruled out intracranial hemorrhage with a negative predictive value of 89.7%, (at a sensitivity for detecting intracranial hemorrhage of 90.0%). Discussion The high negative predictive value of a GFAP test system allows ruling out patients with intracranial hemorrhage. Conclusion In settings where immediate brain imaging is not available, this would enable to implement secondary prevention (e.g., aspirin) in suspected ischemic stroke patients as soon as possible.
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Pierre, Kevin, Vanessa Molina, Shil Shukla, Anthony Avila, Nicholas Fong, Jessica Nguyen, and Brandon Lucke-Wold. "Chronic traumatic encephalopathy: Diagnostic updates and advances." AIMS Neuroscience 9, no. 4 (2022): 519–35. http://dx.doi.org/10.3934/neuroscience.2022030.
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<abstract> <p>Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that occurs secondary to repetitive mild traumatic brain injury. Current clinical diagnosis relies on symptomatology and structural imaging findings which often vary widely among those with the disease. The gold standard of diagnosis is post-mortem pathological examination. In this review article, we provide a brief introduction to CTE, current diagnostic workup and the promising research on imaging and fluid biomarker diagnostic techniques. For imaging, we discuss quantitative structural analyses, DTI, fMRI, MRS, SWI and PET CT. For fluid biomarkers, we discuss p-tau, TREM2, CCL11, NfL and GFAP.</p> </abstract>