Relevant bibliographies by topics / Cerebrospinal fluid, amyotrophic lateral sclerosis, microrna

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters

Academic literature on the topic 'Cerebrospinal fluid, amyotrophic lateral sclerosis, microrna'

Author: Grafiati
Published: 10 March 2023

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Journal articles on the topic "Cerebrospinal fluid, amyotrophic lateral sclerosis, microrna"

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Ricci, Claudia, Carlotta Marzocchi, and Stefania Battistini. "MicroRNAs as Biomarkers in Amyotrophic Lateral Sclerosis." Cells 7, no. 11 (November 20, 2018): 219. http://dx.doi.org/10.3390/cells7110219.

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Amyotrophic lateral sclerosis (ALS) is an incurable and fatal disorder characterized by the progressive loss of motor neurons in the cerebral cortex, brain stem, and spinal cord. Sporadic ALS form accounts for the majority of patients, but in 1–13.5% of cases the disease is inherited. The diagnosis of ALS is mainly based on clinical assessment and electrophysiological examinations with a history of symptom progression and is then made with a significant delay from symptom onset. Thus, the identification of biomarkers specific for ALS could be of a fundamental importance in the clinical practice. An ideal biomarker should display high specificity and sensitivity for discriminating ALS from control subjects and from ALS-mimics and other neurological diseases, and should then monitor disease progression within individual patients. microRNAs (miRNAs) are considered promising biomarkers for neurodegenerative diseases, since they are remarkably stable in human body fluids and can reflect physiological and pathological processes relevant for ALS. Here, we review the state of the art of miRNA biomarker identification for ALS in cerebrospinal fluid (CSF), blood and muscle tissue; we discuss advantages and disadvantages of different approaches, and underline the limits but also the great potential of this research for future practical applications.
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Gentile, Giulia, Giovanna Morello, Valentina La Cognata, Maria Guarnaccia, Francesca Luisa Conforti, and Sebastiano Cavallaro. "Dysregulated miRNAs as Biomarkers and Therapeutical Targets in Neurodegenerative Diseases." Journal of Personalized Medicine 12, no. 5 (May 10, 2022): 770. http://dx.doi.org/10.3390/jpm12050770.

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Alzheimer’s disease (AD), Parkinson’s disease (PD), and Amyotrophic Lateral Sclerosis (ALS) are representative neurodegenerative diseases (NDs) characterized by degeneration of selective neurons, as well as the lack of effective biomarkers and therapeutic treatments. In the last decade, microRNAs (miRNAs) have gained considerable interest in diagnostics and therapy of NDs, owing to their aberrant expression and their ability to target multiple molecules and pathways. Here, we provide an overview of dysregulated miRNAs in fluids (blood or cerebrospinal fluid) and nervous tissue of AD, PD, and ALS patients. By emphasizing those that are commonly dysregulated in these NDs, we highlight their potential role as biomarkers or therapeutical targets and describe the use of antisense oligonucleotides as miRNA therapies.
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Eyileten, Ceren, Lucia Sharif, Zofia Wicik, Daniel Jakubik, Joanna Jarosz-Popek, Aleksandra Soplinska, Marek Postula, Anna Czlonkowska, Agnieszka Kaplon-Cieslicka, and Dagmara Mirowska-Guzel. "The Relation of the Brain-Derived Neurotrophic Factor with MicroRNAs in Neurodegenerative Diseases and Ischemic Stroke." Molecular Neurobiology 58, no. 1 (September 17, 2020): 329–47. http://dx.doi.org/10.1007/s12035-020-02101-2.

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AbstractBrain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family of growth factors that plays a crucial role in the development of the nervous system while supporting the survival of existing neurons and instigating neurogenesis. Altered levels of BDNF, both in the circulation and in the central nervous system (CNS), have been reported to be involved in the pathogenesis of neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD), multiple sclerosis (MS), and ischemic stroke. MicroRNAs (miRNAs) are a class of non-coding RNAs found in body fluids such as peripheral blood and cerebrospinal fluid. Several different miRNAs, and their target genes, are recognized to be involved in the pathophysiology of neurodegenerative and neurovascular diseases. Thus, they present as promising biomarkers and a novel treatment approach for CNS disorders. Currently, limited studies provide viable evidence of miRNA-mediated post-transcriptional regulation of BDNF. The aim of this review is to provide a comprehensive assessment of the current knowledge regarding the potential diagnostic and prognostic values of miRNAs affecting BDNF expression and its role as a CNS disorders and neurovascular disease biomarker. Moreover, a novel therapeutic approach in neurodegenerative diseases and ischemic stroke targeting miRNAs associated with BDNF will be discussed.
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Geekiyanage, Hirosha, Shima Rayatpisheh, James A. Wohlschlegel, Robert Brown, and Victor Ambros. "Extracellular microRNAs in human circulation are associated with miRISC complexes that are accessible to anti-AGO2 antibody and can bind target mimic oligonucleotides." Proceedings of the National Academy of Sciences 117, no. 39 (September 14, 2020): 24213–23. http://dx.doi.org/10.1073/pnas.2008323117.

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MicroRNAs (miRNAs) function cell-intrinsically to regulate gene expression by base-pairing to complementary mRNA targets while in association with Argonaute, the effector protein of the miRNA-mediated silencing complex (miRISC). A relatively dilute population of miRNAs can be found extracellularly in body fluids such as human blood plasma and cerebrospinal fluid (CSF). The remarkable stability of circulating miRNAs in such harsh extracellular environments can be attributed to their association with protective macromolecular complexes, including extracellular vesicles (EVs), proteins such as Argonaut 2 (AGO2), or high-density lipoproteins. The precise origins and the potential biological significance of various forms of miRNA-containing extracellular complexes are poorly understood. It is also not known whether extracellular miRNAs in their native state may retain the capacity for miRISC-mediated target RNA binding. To explore the potential functionality of circulating extracellular miRNAs, we comprehensively investigated the association between circulating miRNAs and the miRISC Argonaute AGO2. Using AGO2 immunoprecipitation (IP) followed by small-RNA sequencing, we find that miRNAs in circulation are primarily associated with antibody-accessible miRISC/AGO2 complexes. Moreover, we show that circulating miRNAs can base-pair with a target mimic in a seed-based manner, and that the target-bound AGO2 can be recovered from blood plasma in an ∼1:1 ratio with the respective miRNA. Our findings suggest that miRNAs in circulation are largely contained in functional miRISC/AGO2 complexes under normal physiological conditions. However, we find that, in human CSF, the assortment of certain extracellular miRNAs into free miRISC/AGO2 complexes can be affected by pathological conditions such as amyotrophic lateral sclerosis.
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Nakayama, Yui, Satoru Morimoto, Misao Yoneda, Shigeki Kuzuhara, and Yasumasa Kokubo. "Cerebrospinal Fluid Biomarkers for Kii Amyotrophic Lateral Sclerosis/Parkinsonism-Dementia Complex." Journal of Neurodegenerative Diseases 2013 (March 27, 2013): 1–4. http://dx.doi.org/10.1155/2013/679089.

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Objective. Amyotrophic lateral sclerosis/parkinsonism-dementia complex is classified as one of the tauopathies. Methods. The total tau, phosphorylated tau, and amyloid β42 levels were assayed in cerebrospinal fluid from patients with Kii amyotrophic lateral sclerosis/parkinsonism-dementia complex (), Alzheimer’s disease (), Parkinson’s disease (), amyotrophic lateral sclerosis (), and controls () using specific enzyme-linked immunosorbent assay methods. Results. Total tau and phosphorylated tau did not increase and amyloid β42 was relatively reduced in Kii amyotrophic lateral sclerosis/parkinsonism-dementia complex. Relatively reduced amyloid β42 might discriminate Kii amyotrophic lateral sclerosis/parkinsonism-dementia complex from amyotrophic lateral sclerosis and Parkinson’s disease, and the ratios of phosphorylated-tau to amyloid β42 could discriminate Kii amyotrophic lateral sclerosis/parkinsonism-dementia complex from Alzheimer’s disease. Conclusions. Cerebrospinal fluid analysis may be useful to differentiate amyotrophic lateral sclerosis/parkinsonism-dementia complex from Alzheimer’s disease, amyotrophic lateral sclerosis, and Parkinson’s disease.
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Matías-Guiu, J., L. Galán, R. García-Ramos, J. A. Barcia, and A. Guerrero. "Cerebrospinal fluid cytotoxicity in lateral amyotrophic sclerosis." Neurología (English Edition) 25, no. 6 (2010): 364–73. http://dx.doi.org/10.1016/s2173-5808(10)70068-7.

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Finsterer, Josef, and Bruno Mamoli. "Cerebrospinal fluid filtration in amyotrophic lateral sclerosis." European Journal of Neurology 6, no. 5 (September 1999): 597–600. http://dx.doi.org/10.1046/j.1468-1331.1999.650597.x.

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Brettschneider, Johannes, Karin Widl, Dagmar Schattauer, Albert C. Ludolph, and Hayrettin Tumani. "Cerebrospinal fluid erythropoietin (EPO) in amyotrophic lateral sclerosis." Neuroscience Letters 416, no. 3 (April 2007): 257–60. http://dx.doi.org/10.1016/j.neulet.2007.02.002.

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Kornhuber, Malte E., and Johannes Kornhuber. "Cerebrospinal fluid amino acids in amyotrophic lateral sclerosis." Annals of Neurology 31, no. 4 (April 1992): 449. http://dx.doi.org/10.1002/ana.410310418.

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Thompson, Alexander G., Elizabeth Gray, Marie-Laëtitia Thézénas, Philip D. Charles, Samuel Evetts, Michele T. Hu, Kevin Talbot, Roman Fischer, Benedikt M. Kessler, and Martin R. Turner. "Cerebrospinal fluid macrophage biomarkers in amyotrophic lateral sclerosis." Annals of Neurology 83, no. 2 (February 2018): 258–68. http://dx.doi.org/10.1002/ana.25143.

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Dissertations / Theses on the topic "Cerebrospinal fluid, amyotrophic lateral sclerosis, microrna"

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Kostesky, Trisha Ehren. "A study of potential sporadic amyotrophic lateral sclerosis biomarkers in cerebrospinal fluid." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/35690.

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Sporadic Amyotrophic Lateral Sclerosis (sALS) is a debilitating and fatal neurodegenerative disease of unknown etiology. It currently has no biochemical marker to confirm a clinical diagnosis, and this has negative consequences for patients when it comes to initiating early medical intervention and participating in therapeutic trials. Valid biomarkers can be useful for diagnostic and prognostic indications as well as providing insight into disease pathogenesis and identifying targets for therapeutic interventions. Cerebrospinal fluid (CSF) may be a particularly valuable source of biomarkers because it is in close anatomical proximity to the brain and spinal cord, thus making it a better reflection of biochemical alterations resulting from neurodegenerative disease. This study examined the proteome profile of CSF from sALS patients and controls to identify candidate biomarkers that might aid in the diagnosis of sALS and possibly provide insight into disease pathogenesis. An antibody microarray technique was used to measure the expression levels of various cell signalling proteins in the CSF of sALS patients and healthy controls. The results identified a number of protein changes in sALS CSF, including a considerable decrease in the level of ephrin type-A receptor 1 tyrosine kinase (EphA1) relative to control CSF. Follow-up validation studies by Western blotting with CSF samples from a separate cohort of 19 sALS patients, 21 healthy controls and 10 neurological disease controls confirmed a statistically significant decrease in EphA1 levels. As a diagnostic test, EphA1 levels in CSF had a statistically significant ability to discriminate between sALS patients and controls. Receptor levels also had a positive correlation with age at onset of sALS symptoms, indicating that this potential biomarker may be capable of identifying people who are prone to an earlier onset of disease. The Eph family of tyrosine kinase receptors engage in complex bidirectional signalling that functions as a major form of contact-dependent communication between cells, and mediates a variety of cellular responses. As research begins to further elucidate these multifaceted signalling mechanisms, imbalances in Eph receptor functioning are increasingly implicated in a variety of pathologies in the central nervous system that are related to some of the major features of ALS.
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Zetterström, Per. "Misfolded superoxide dismutase-1 in amyotrophic lateral sclerosis." Doctoral thesis, Umeå universitet, Klinisk kemi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-43898.

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Amyotrophic lateral sclerosis (ALS) is a disease in which the motor neurons die in a progressive manner, leading to paralysis and muscle wasting. ALS is always fatal, usually through respiratory failure when the disease reaches muscles needed for breathing. Most cases are sporadic, but approximately 5–10% are familial. The first gene to be linked to familial ALS encodes the antioxidant enzyme superoxide dismutase-1 (SOD1). Today, more than 160 different mutations in SOD1 have been found in ALS patients.  The mutant SOD1 proteins cause ALS by gain of a toxic property that should be common to all. Aggregates of SOD1 in motor neurons are hallmarks of ALS patients and transgenic models carrying mutant SOD1s, suggesting that misfolding, oligomerization, and aggregation of the protein may be involved in the pathogenesis. SOD1 is normally a very stable enzyme, but the structure has several components that make SOD1 sensitive to misfolding. The aim of the work in this thesis was to study misfolded SOD1 in vivo. Small amounts of soluble misfolded SOD1 were identified as a common denominator in transgenic ALS models expressing widely different forms of mutant SOD1, as well as wild-type SOD1. The highest levels of misfolded SOD1 were found in the vulnerable spinal cord. The amounts of misfolded SOD1 were similar in all the different models and showed a broad correlation with the lifespan of the different mouse strains. The misfolded SOD1 lacked the C57-C146 intrasubunit disulfide bond and the stabilizing zinc and copper ions, and was prinsipally monomeric. Forms with higher apparent molecular weights were also found, some of which might be oligomers. Misfolding-prone monomeric SOD1 appeared to be the principal source of misfolded SOD1 in the CNS. Misfolded SOD1 in the spinal cord was found to interact mainly with chaperones, with Hsc70 being the most important. Only a minor proportion of the Hsc70 was sequestered by SOD1, however, suggesting that chaperone depletion is not involved in ALS.  SOD1 is normally found in the cytoplasm but can be secreted. Extracellular mutant SOD1 has been found to be toxic to motor neurons and glial cells. Misfolded SOD1 in the extracellular space could be involved in the spread of the disease between different areas of the CNS and activate glial cells known to be important in ALS. The best way to study the interstitium of the CNS is through the cerebrospinal fluid (CSF), 30% of which is derived from the interstitial fluid. Antibodies specific for misfolded SOD1 were used to probe CSF from ALS patients and controls for misfolded SOD1. We did find misfolded SOD1 in CSF, but at very low levels, and there was no difference between ALS patients and controls. This argues against there being a direct toxic effect of extracellular SOD1 in ALS pathogenesis. In conclusion, soluble misfolded SOD1 is a common denominator for transgenic ALS model mice expressing widely different mutant SOD1 proteins. The misfolded SOD1 is mainly monomeric, but also bound to chaperones, and possibly exists in oligomeric forms also. Misfolded SOD1 in the interstitium might promote spread of aggregation and activate glial cells, but it is too scarce to directly cause cytotoxicity.
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Jonsson, P. Andreas. "Superoxide dismutase 1 and amyotrophic lateral sclerosis." Doctoral thesis, Umeå : Medical Biosciences, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-611.

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Grundström, Eva. "On pathophysiological mechanisms in amyothrophic lateral sclerosis." Doctoral thesis, Uppsala University, Department of Neuroscience, 2000. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-521.

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Amyotrophic lateral sclerosis is a fatal, progressive neurodegenerative disease with unknown ethiology. The aim of this study was to increase understanding of the pathophysiological mechanisms of dying motor neurons and wasting muscle tissue in this particular disorder.

Quantitative receptor autoradiographic methodology was applied on cervical spinal cord sections from patients with ALS to evaluate the specific binding of the acetylcholine transporter 3H-vesamicol in motor neurons. Despite a significant reduction of the number of ventral motor neurons in ALS, the 3H-vesamicol binding was not reduced in ALS compared to control cases, which suggests an increased metabolic activity in remaining motor neurons.

Motor neurons dying in ALS might go through apoptosis (programmed cell death), so immunohistochemical and TUNEL techniques were applied on thoracic spinal cord from ALS patients to evaluate the possibility of an apoptotic process. The increased Bax expression indicates an apoptotic process and further, motor neurons were TUNEL-positive, indicating DNA degradation caused by programmed cell death.

Muscle biopsies were obtained from ALS patients, and mRNA levels for the neurotrophic factors GDNF and BDNF were measured and compared to control subjects. GDNF levels were increased in muscle tissue in ALS whereas BDNF levels were unaltered.

Levels of GDNF and BDNF were also measured in cerebrospinal fluid from ALS patients and controls using ELISA methodology. Levels of BDNF were unaltered in ALS cornpared to controls. GDNF however was not detectable in controls whereas 12 out of 15 ALS patients had measurab1e levels of GDNW. A marked upregulation of endogenous GDNF and GDNF mRNA in ALS CSF and muscle respectively is of special interest in relation to clinical trials where GDNF is administered to this group of patients.

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Johansson, Anders. "Search for biomarkers in ALS and Parkinson's Disease positron emission tomography and cerebrospinal fluid studies /." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univeritetsbiblioteket [distributör], 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-102040.

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Wuolikainen, Anna. "Metabolomics studies of ALS a multivariate search for clues about a devastating disease /." Doctoral thesis, Umeå : Department of Pharmacology and Clinical Neuroscience, Umeå university, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-26894.

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Ramström, Margareta. "Analysis of Complex Biological Samples using Liquid Chromatography-Fourier Transform Ion Cyclotron Resonance Mass Spectrometry." Doctoral thesis, Uppsala University, Analytical Chemistry, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5729.

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Studies of protein and peptide expression are vital in order to understand complex biological systems. As demonstrated in this thesis, on-line packed capillary liquid chromatography-Fourier transform ion cyclotron resonance mass spectrometry (LC-FTICR MS) is a useful analytical tool for such studies.

A proteomics method, based on global tryptic digestion and subsequent separation and detection of the peptides by LC-FTICR MS, was developed for qualitative analysis of body fluids. Initial experiments on cerebrospinal fluid (CSF) provided results that were comparable or superior to those achieved by more time- and sample-consuming techniques. The method was also successfully applied on plasma and amniotic fluid. One of the major challenges in proteomics is the broad dynamic range of proteins in biological matrices. The advantages of removing high-abundant components from CSF and plasma prior to MS were demonstrated.

In order to search for potential biomarkers, mass chromatograms of CSF from patients suffering from amyotrophic lateral sclerosis (ALS) and controls were compared using an in-house constructed pattern recognition program. ALS-specific patterns were observed, and four out of five unknown samples were correctly assigned. Alternative strategies to quantitatively compare two pools of samples rely on differential chemical labeling. The performance of one such method, quantification-using-enhanced-signal-tags, was investigated in complex sample analysis. The experimental intensity ratios were proven to be consistent with the prepared concentration ratios of abundant proteins in CSF.

Finally, the thesis reports on the first experiments where electron capture dissociation (ECD) was successfully incorporated in on-line LC-MS experiments. ECD and nozzle-skimmer fragmentation were applied to a sample of endocrine peptides extracted from mouse pancreatic islets. The two fragmentation methods provided complementary information. However, the method needs further optimization before it can be applied in the analysis of more complex samples, such as body fluids.

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Lind, Anne-Li. "Biomarkers for Better Understanding of the Pathophysiology and Treatment of Chronic Pain : Investigations of Human Biofluids." Doctoral thesis, Uppsala universitet, Anestesiologi och intensivvård, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-326180.

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Chronic pain affects 20 % of the global population, causes suffering, is difficult to treat, and constitutes a large economic burden for society. So far, the characterization of molecular mechanisms of chronic pain-like behaviors in animal models has not translated into effective treatments. In this thesis, consisting of five studies, pain patient biofluids were analyzed with modern proteomic methods to identify biomarker candidates that can be used to improve our understanding of the pathophysiology chronic pain and lead to more effective treatments. Paper I is a proof of concept study, where a multiplex solid phase-proximity ligation assay (SP-PLA) was applied to cerebrospinal fluid (CSF) for the first time. CSF reference protein levels and four biomarker candidates for ALS were presented. The investigated proteins were not altered by spinal cord stimulation (SCS) treatment for neuropathic pain. In Paper II, patient CSF was explored by dimethyl and label-free mass spectrometric (MS) proteomic methods. Twelve proteins, known for their roles in neuroprotection, nociceptive signaling, immune regulation, and synaptic plasticity, were identified to be associated with SCS treatment of neuropathic pain. In Paper III, proximity extension assay (PEA) was used to analyze levels of 92 proteins in serum from patients one year after painful disc herniation. Patients with residual pain had significantly higher serum levels of 41 inflammatory proteins. In Paper IV, levels of 55 proteins were analyzed by a 100-plex antibody suspension bead array (ASBA) in CSF samples from two neuropathic pain patient cohorts, one cohort of fibromyalgia patients and two control cohorts. CSF protein profiles consisting of levels of apolipoprotein C1, ectonucleotide pyrophosphatase/phosphodiesterase family member 2, angiotensinogen, prostaglandin-H2 D-isomerase, neurexin-1, superoxide dismutases 1 and 3 were found to be associated with neuropathic pain and fibromyalgia. In Paper V, higher CSF levels of five chemokines and LAPTGF-beta-1were detected in two patient cohorts with neuropathic pain compared with healthy controls. In conclusion, we demonstrate that combining MS proteomic and multiplex antibody-based methods for analysis of patient biofluid samples is a viable approach for discovery of biomarker candidates for the pathophysiology and treatment of chronic pain. Several biomarker candidates possibly reflecting systemic inflammation, lipid metabolism, and neuroinflammation in different pain conditions were identified for further investigation.
Uppsala Berzelii Technology Centre for Neurodiagnostics
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CORRADETTI, RENATO. "Cerebrospinal fluid and serum miRNAs in sporadic amyotrophic lateral sclerosis: potential biomarkers and pathogenic role." Doctoral thesis, 2016. http://hdl.handle.net/2158/1036322.

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Amyotrophic lateral sclerosis (ALS) is a progressive, fatal neurodegenerative disorder. Since there is no diagnostic laboratory test, the identification of biomarkers specific for ALS could be of fundamental importance in clinical practice. In the last few years microRNAs (miRNAs) have aroused great interest as potential biomarkers for neurodegenerative diseases in serum and cerebrospinal fluid (CSF) samples. In particular, miRNAs detected in (CSF) better reflect brain pathological conditions than those present in other body fluids but its withdrawal is more invasive compare to blood. The aim of the study was to identify a serum and CSF miRNA set that could differentiate ALS from non-ALS condition. We performed miRNA profiling in CSF and serum from ALS patients (n=24; eight with C9orf72 expansion) and unaffected control subjects (n=24) by quantitative reverse transcription PCR (q-RT-PCR) on a 372-miRNA PCR array. Thirteen downregulated miRNAs and one upregulated miRNAs and eighteen deregulated miRNAs, one downregulated and two upregulated were identified in ALS from CSF and serum samples respectively. In validation experiments, among the deregulated miRNAs, eight were confirmed as significantly deregulated in CSF samples from patients compared to controls and three were confirmed in serum samples. No significant differences were observed between ALS patients with or without C9orf72 expansion neither for CSF nor for serum samples. The Receiver Operator Characteristic (ROC) curve analyses revealed for CSF samples the highest diagnostic accuracy as potential ALS biomarkers for the upregulated miR181a-5p and the downregulated miR21-5p and miR15b-5p. The analyses of miR181a-5p/miR21-5p and miR181a-5p/miR15b-5p ratios were able to detect ALS with 90% and 85% sensitivity and 87% and 91% specificity, respectively, confirming the application potential of these molecules as disease biomarkers. Moreover, pathway analysis indicated that these deregulated miRNAs are implicated in apoptotic way, providing important insight into disease processes responsible for motor neuron degeneration.
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Findlater, Joseph. "Peripherin-28 as a Biomarker of ALS: A Methodological Study." Thesis, 2010. http://hdl.handle.net/1807/25578.

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Amyotrophic lateral sclerosis (ALS) is a progressive and fatal neurodegenerative disease which currently lacks rapid and definitive diagnostic tests. Recently identified neuron specific splice variant molecules, Per28 and NFL-60, have been shown to contain unique epitopes and to have altered levels of expression in ALS patients. It is believed that these factors make Per28 and NFL-60 excellent candidate biomarkers for the ALS disease state. In this study, we attempted to develop ELISA assays directed against Per28 and NFL-60, as well as a generalized guideline for splice variant ELISA development, which could be used in a clinical setting. Limitations in currently identified antibodies to the splice variants allowed only for the completion of a Per28 ELISA, which lacked the sensitivity for clinical relevance. This assay creation process, however, did produce a guideline for similar ELISA development, which should allow for the more expeditious creation future ELISA.
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Book chapters on the topic "Cerebrospinal fluid, amyotrophic lateral sclerosis, microrna"

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Silani, V., A. Pizzuti, L. M. Redaelli, R. Bassani, I. R. Causarano, M. Buscaglia, G. Zuliani, and G. Scarlato. "ALS Cerebrospinal Fluid Enhances Human Foetal Astroglial Cell Proliferation in Vitro." In Amyotrophic Lateral Sclerosis, 79–81. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5302-7_13.

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Bowser, Robert, James Connor, and Martin Turner. "Cerebrospinal fluid-based biomarkers for amyotrophic lateral sclerosis." In Amyotrophic Lateral Sclerosis and the Frontotemporal Dementias, 249–63. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199590674.003.0017.

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Wormser, Uri, Jessica Mandrioli, Marco Vinceti, Nicola Fini, Amnon Sintov, Berta Brodsky, Elena Proscura, and Yoram Finkelstein. "Analysis of Cerebrospinal Fluid of Amyotrophic Lateral Sclerosis Patients: Reduction in Alpha-1-antitrypsin and Increase in IL-23." In Perspective of Recent Advances in Medical Research Vol. 10, 89–101. B P International (a part of SCIENCEDOMAIN International), 2023. http://dx.doi.org/10.9734/bpi/pramr/v10/4520e.

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Ahmad Malik, Jonaid, Jeba AjgarAnsari, Sakeel Ahmed, Archana Rani, Shabana Yasmeen Ansari, and Sirajudheen Anwar. "Emerging Selenium Nanoparticles for CNS Intervention." In Biomedical Engineering. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.109418.

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Central nervous system (CNS) diseases have seriously impacted human wellness for the past few decades, specifically in developing countries, due to the unavailability of successful treatment. Due to the blood-brain barrier (BBB) and blood-cerebrospinal fluid barrier transport of drug and treatment of CNS disorders has become difficult. Nanoscale materials like Selenium nanoparticles (SeNPs) offer a possible therapeutic strategy for treating brain diseases like Alzheimer’s, Frontotemporal dementia, Amyotrophic lateral sclerosis, Epilepsy, Parkinson’s disease, and Huntington’s disease. After being functionalized with active targeting ligands, SeNPs are versatile and competent in conveying combinations of cargoes to certain targets. We shall pay close attention to the primarily targeted therapies for SeNPs in CNS diseases. The objective of this paper was to highlight new developments in the exploration of SeNP formation and their potential applications in the management of CNS diseases. Furthermore, we also discussed the mechanisms underlying management of CNS disease, several therapeutic potentials for SeNPs, and the results of their preclinical research using diverse animal models. These methods might lead to better clinical and diagnostic results.
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