Journal articles: 'Neutrophils, Alzheimer's disease'

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Zenaro, Elena, Enrica Pietronigro, Vittorina Della Bianca, Gennj Piacentino, Alessio Montresor, Ermanna Turano, Bruno Bonetti, and Gabriela Constantin. "Neutrophils induce Alzheimer's-like disease via LFA-1-integrin and neutrophil extracellular traps." Journal of Neuroimmunology 275, no. 1-2 (October 2014): 145. http://dx.doi.org/10.1016/j.jneuroim.2014.08.389.

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Baik, Sung Hoon, Moon-Yong Cha, Young-Min Hyun, Hansang Cho, Bashar Hamza, Dong Kyu Kim, Sun-Ho Han, et al. "Migration of neutrophils targeting amyloid plaques in Alzheimer's disease mouse model." Neurobiology of Aging 35, no. 6 (June 2014): 1286–92. http://dx.doi.org/10.1016/j.neurobiolaging.2014.01.003.

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Garlind, Anita, Eva Nilsson, and Jan Palmblad. "Calcium ion transients in neutrophils from patients with sporadic Alzheimer's disease." Neuroscience Letters 255, no. 2 (September 1998): 95–98. http://dx.doi.org/10.1016/s0304-3940(98)00716-2.

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Zenaro, Elena, Gabriela Constantin, Enrica Pietronigro, Vittorina Della Bianca, Gennj Piacentino, Ermanna Turano, Alessio Montresor, Carlo Laudanna, and Bruno Bonetti. "O2-06-05: NEUTROPHILS INDUCE ALZHEIMER'S-LIKE DISEASE VIA LFA-1-INTEGRIN AND NEUTROPHIL EXTRACELLULAR TRAPS." Alzheimer's & Dementia 10 (July 2014): P175—P176. http://dx.doi.org/10.1016/j.jalz.2014.04.190.

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D'Cruz, Akshay A., Meghan Bliss-Moreau, Maria Ericcson, and Ben A. Croker. "Mlkl Pores Release Neutrophil Extracellular Traps in Necroptotic Neutrophils." Blood 126, no. 23 (December 3, 2015): 2200. http://dx.doi.org/10.1182/blood.v126.23.2200.2200.

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Abstract Neutrophil extracellular traps (NETs) are networks of extracellular nuclear DNA and microbicidal proteins released from neutrophils in response to tissue damage and infection. Despite evidence of pathogenic roles for NETs in systemic lupus erythematosus, rheumatoid arthritis, diabetes, artherosclerosis and Alzheimer's disease, the major biochemical pathways controlling their formation remains poorly understood. Apoptosis does not contribute to NET formation but the role of regulated non-apoptotic cell death pathways such as necroptosis is not known. We have investigated the role of positive and negative regulators of necroptosis including receptor-interacting protein kinase-3 (RIPK3), mixed lineage kinase domain-like (MLKL), receptor-interacting protein kinase-1 (RIPK1) and Caspase-8. Using immunogold electron microscopy, flow cytometry, imaging flow cytometry and fluorescence microscopy, we demonstrate that necroptosis can drive NET formation via MLKL pore formation at the cell surface. This process is caspase-independent but reactive oxygen species-dependent. Genetically-modified mouse peripheral blood and bone marrow neutrophils were used to show that Caspase-8 and RIPK1 negatively regulate NET formation driven by RIPK3 and MLKL. Mice that lack MLKL are deficient in necroptosis and NET formation, and were sensitive to methicillin-resistant Staphylococcus aureus (MRSA). Neutrophil-specific Caspase-8-deficiency also leads to increased susceptibility to MRSA due to increased rates of necroptotic neutrophil death. Killing of MRSA by necroptotic neutrophils is sensitive to DNase, and is dependent on MLKL, suggesting that necroptosis-driven NET formation contributes to the bactericidal activity of neutrophils. Human peripheral blood neutrophils also generate NETs that are sensitive to pharmacological inhibitors of necroptosis, suggesting that targeting necroptosis in general may help combat autoimmune responses to DNA. This study provides a framework to investigate the role of extracellular DNA release and cell death in the setting of infection, autoimmunity and autoinflammatory disease. Disclosures No relevant conflicts of interest to declare.

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LE PAGE, Aurélie, Julie Lamoureux, Karine Bourgade, Eric Frost, Gilles Dupuis, and Tamas Fulop. "Immune signatures of Alzheimer’s disease: profiles of neutrophils. (HUM1P.301)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 52.26. http://dx.doi.org/10.4049/jimmunol.194.supp.52.26.

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Abstract Alzheimer's disease (AD) is the most common form of dementia. Amyloïd plaques accumulation and microbial infections have been proposed as an important components of AD aetiology. Defects in amyloïd-β clearance by monocyte/macrophage/microglia, imply that the immune system may participate in development and progression of AD. Phenotype and functional analysis of polymorphonuclear neutrophils (PMN) in peripheral blood were performed by flow cytometry. Our cohort of patients comprised amnestic Mild Cognitive Impairment (aMCI) (n = 10), mild stage AD (mAD) (n = 10) and healthy elderly controls (n = 10). aMCI patients had memory impairment but no functional disorders. However, these patients have a 50% chance of developing AD within 3 years following the diagnostic. PMN number was unchanged between the three groups. In contrast, the CD177+ population was significantly increased in mAD patients (p < 0.05). Phagocytosis of opsonized bacteria was less in aMCI and AD patients than controls. This observation was associated in aMCI with a decrease in CD33 (siglec 3) and complement receptor for C5A expression. Decreased expression of CD14 (a pattern recognition receptor), CD15 (carbohydrate adhesion molecule) and CD16 (FcγRIII) expression was found in mAD patients. Our results describe for the first time alterations of neutrophils in aMCI patients. PMN analysis may provide a useful tool in early identification of AD patients.

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Zenaro, Elena, Enrica Pietronigro, Vittorina Della Bianca, Gennj Piacentino, Laura Marongiu, Simona Budui, Ermanna Turano, et al. "Neutrophils promote Alzheimer's disease–like pathology and cognitive decline via LFA-1 integrin." Nature Medicine 21, no. 8 (July 27, 2015): 880–86. http://dx.doi.org/10.1038/nm.3913.

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Eckert, Anne, Hans Förstl, Rainer Zerfass, Henrike Hartmann, and Walter E. Müller. "Lymphocytes and neutrophils as peripheral models to study the effect of β-amyloid on cellular calcium signalling in Alzheimer's disease." Life Sciences 59, no. 5-6 (July 1996): 499–510. http://dx.doi.org/10.1016/0024-3205(96)00329-3.

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Ivanov, P. A., A. A. Shmakova, and N. M. Mikhailova. "NEUTROPHILS’ FUNCTIONAL STATE IN ALZHEIMER’S DISEASE." Medical academic journal 19, no. 1S (December 15, 2019): 81–82. http://dx.doi.org/10.17816/maj191s181-82.

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Alzheimer’s disease (AD) is the most widespread neurodegenerative disease of older age, which is associated with the deposition of amyloid-beta polymerized peptide (consisting of 42 amino-acid residues) in the brain. The microglial phagocytosis disturbance, which is observed during AD, is possibly the key factor in the process. The research of neutrophils in patients with AD is of special interest due to the pressing problem of finding peripheral markers of AD. Analysis of neutrophils’ functional state in patients with AD is the objective of the present study. A reliable decrease of neutrophils’ phagocytic activity was established in group of patients with AD in comparison with control group (p < 0,05) (PI = 1.16 [0.64; 2.68] and PI = 2.34 [2.06; 2.85], respectively). A reliable increase of leukocytic elastase (LE) enzymatic activity (p < 0.05) was discovered in neutrophil lysate in AD group compared to control (LE = 0.43 [0.29; 0.77] and 0.29 [0.26; 0.38], respectively) at the same time. Comparison of PI and LE indicators in neutrophils’ lysate of AD group showed negative correlation between these parameters (r = 0.49, p < 0.05), which means that phagocytosis reduction during AD is accompanied by simultaneous LE activity increase in lysate of these cells.The obtained results allow to draw a conclusion that neutrophils’ phagocytic activity decreases during AD. Thus, discovered changes in neutrophils’ functional state can be considered as a potential peripheral AD marker.

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Rivero-Pino, Fernando, Elena Grao-Cruces, Soledad Lopez-Enriquez, Gonzalo Alba, Elvira Marquez-Paradas, Carmen M. Claro-Cala, Consuelo Santa-Maria, and Sergio Montserrat-de la Paz. "Modulation of Beta-Amyloid-Activated Primary Human Neutrophils by Dietary Phenols from Virgin Olive Oil." Nutrients 15, no. 4 (February 14, 2023): 941. http://dx.doi.org/10.3390/nu15040941.

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The defense mechanism against harmful stimuli is inflammation. Indeed, neurodegenerative disorders can arise as a result of a persistent neuroinflammation. Beta-amyloid (Aβ1-42) is an early trigger in the origination of Alzheimer’s disease, leading to synaptic and cognitive impairments. Virgin olive oil (VOO) is correlated with a decreased risk of developing immune-inflammatory disorders, but the potential effects of the phenolic fraction (PF) from VOO in the modulation of neuroinflammatory processes in neutrophils remain unknown. In this study, we investigated the ability of the PF to modulate the activation of Aβ1-42-stimulated primary human neutrophils, focusing on the expression of gene and surface markers and the release of pro-inflammatory and chemoattractant mediators. Down-regulation of pro-inflammatory cytokine gene expression in Aβ1-42-treated neutrophils, among other changes, was reported. Furthermore, pretreatment with PF prevented neutrophil activation. The beneficial effects in the modulation of inflammatory responses show the relevance of VOO to achieve a healthier diet that can help prevent inflammatory diseases.

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Rusek, Marta, Joanna Smith, Kamel El-Khatib, Kennedy Aikins, Stanisław J. Czuczwar, and Ryszard Pluta. "The Role of the JAK/STAT Signaling Pathway in the Pathogenesis of Alzheimer’s Disease: New Potential Treatment Target." International Journal of Molecular Sciences 24, no. 1 (January 3, 2023): 864. http://dx.doi.org/10.3390/ijms24010864.

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Alzheimer’s disease is characterized by the accumulation of amyloid plaques and neurofibrillary tangles in the brain. However, emerging evidence suggests that neuroinflammation, mediated notably by activated neuroglial cells, neutrophils, and macrophages, also plays an important role in the pathogenesis of Alzheimer’s disease. Therefore, understanding the interplay between the nervous and immune systems might be the key to the prevention or delay of Alzheimer’s disease progression. One of the most important mechanisms determining gliogenic cell fate is the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway that is influenced by the overactivation of microglia and astrocytes. The JAK/STAT signaling pathway is one of the critical factors that promote neuroinflammation in neurodegenerative diseases such as Alzheimer’s disease by initiating innate immunity, orchestrating adaptive immune mechanisms, and finally, constraining neuroinflammatory response. Since a chronic neuroinflammatory environment in the brain is a hallmark of Alzheimer’s disease, understanding the process would allow establishing the underlying role of neuroinflammation, then estimating the prognosis of Alzheimer’s disease development and finding a new potential treatment target. In this review, we highlight the recent advances in the potential role of JAK/STAT signaling in neurological diseases with a focus on discussing future research directions regarding novel therapeutic approaches and predictive biomarkers for Alzheimer’s disease.

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Dong, Yuan, Julien Lagarde, Laura Xicota, Hélène Corne, Yannick Chantran, Thomas Chaigneau, Bruno Crestani, et al. "Neutrophil hyperactivation correlates with Alzheimer's disease progression." Annals of Neurology 83, no. 2 (February 2018): 387–405. http://dx.doi.org/10.1002/ana.25159.

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Vázquez-Villaseñor, Irina, Cynthia I. Smith, Yung J. R. Thang, Paul R. Heath, Stephen B. Wharton, Daniel J. Blackburn, Victoria C. Ridger, and Julie E. Simpson. "RNA-Seq Profiling of Neutrophil-Derived Microvesicles in Alzheimer’s Disease Patients Identifies a miRNA Signature That May Impact Blood–Brain Barrier Integrity." International Journal of Molecular Sciences 23, no. 11 (May 25, 2022): 5913. http://dx.doi.org/10.3390/ijms23115913.

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(1) Background: Systemic infection is associated with increased neuroinflammation and accelerated cognitive decline in AD patients. Activated neutrophils produce neutrophil-derived microvesicles (NMV), which are internalised by human brain microvascular endothelial cells and increase their permeability in vitro, suggesting that NMV play a role in blood–brain barrier (BBB) integrity during infection. The current study investigated whether microRNA content of NMV from AD patients is significantly different compared to healthy controls and could impact cerebrovascular integrity. (2) Methods: Neutrophils isolated from peripheral blood samples of five AD and five healthy control donors without systemic infection were stimulated to produce NMV. MicroRNAs isolated from NMV were analysed by RNA-Seq, and online bioinformatic tools were used to identify significantly differentially expressed microRNAs in the NMV. Target and pathway analyses were performed to predict the impact of the candidate microRNAs on vascular integrity. (3) Results: There was no significant difference in either the number of neutrophils (p = 0.309) or the number of NMV (p = 0.3434) isolated from AD donors compared to control. However, 158 microRNAs were significantly dysregulated in AD NMV compared to controls, some of which were associated with BBB dysfunction, including miR-210, miR-20b-5p and miR-126-5p. Pathway analysis revealed numerous significantly affected pathways involved in regulating vascular integrity, including the TGFβ and PDGFB pathways, as well as Hippo, IL-2 and DNA damage signalling. (4) Conclusions: NMV from AD patients contain miRNAs that may alter the integrity of the BBB and represent a novel neutrophil-mediated mechanism for BBB dysfunction in AD and the accelerated cognitive decline seen as a result of a systemic infection.

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Kalelioglu, T., M. Yuruyen, G. Gultekin, H. Yavuzer, Y. Ozturk, M. Kurt, Y. Topcu, A. Doventas, and M. Emul. "The Neutrophil and Platelet to Lymphocyte Ratios in People with Subjective, Mild Cognitive Impairment and Early Alzheimer's Disease." European Psychiatry 41, S1 (April 2017): S655. http://dx.doi.org/10.1016/j.eurpsy.2017.01.1099.

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BackgroundIn this study we aimed to explore the role of inflammation in subjects with mild Alzheimer dementia (AD), mild cognitive impairment (MCI) and subjective cognitive decline (SCD) via new potential inflammation markers of Neutrophil-lymphocyte ratio (NLR) and Platelet-lymphocyte ratio (PLR). NLR and PLR are useful and cost-effective biomarkers, showing peripheral systemic inflammation, were previously shown in neuropsychiatric disorders [1].MethodsIn screening phase the patients were assessed with mini-mental state examination, clinical dementia rating scale (CDR), geriatric depression scale (GDS) and Hachinski Ischemic Scale (HIS) after unstructured psychiatric interview according to diagnostic and statistical manual of mental disorder, Text Revised (DSM-IV, TR). Spectrum of cognitive decline includes 31 patients with mild Alzheimer's disease, 30 subjects with mild cognitive impairment, 31 individuals with subjective cognitive decline. Thirty-one healthy controls enrolled to the study.ResultsNLR value of patients with AD was 2.38 ± 0.81, subjects with MCI was 2.48 ± 1.19, SCD group was 2.24 ± 1.11 and control group was 1.85 ± 0.80. NLR was significantly higher in AD and MCI groups when compared with control group (P = 0.006, P = 0.03, respectively). Platelet-lymphocyte ratio was not correlated with cognitive impairment. Neutrophil counts were indifferent when comparing either of groups. Lymphocyte levels were significantly lower in each of cognitive decline groups when compared to healthy controls.ConclusionThe present findings suggest that systemic inflammation may have a role in developing Alzheimer's Disease.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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Croasdell, Amanda, Parker F. Duffney, Nina Kim, Shannon H. Lacy, Patricia J. Sime, and Richard P. Phipps. "PPARγand the Innate Immune System Mediate the Resolution of Inflammation." PPAR Research 2015 (2015): 1–20. http://dx.doi.org/10.1155/2015/549691.

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The resolution of inflammation is an active and dynamic process, mediated in large part by the innate immune system. Resolution represents not only an increase in anti-inflammatory actions, but also a paradigm shift in immune cell function to restore homeostasis. PPARγ, a ligand activated transcription factor, has long been studied for its anti-inflammatory actions, but an emerging body of literature is investigating the role of PPARγand its ligands (including thiazolidinediones, prostaglandins, and oleanolic acids) in all phases of resolution. PPARγcan shift production from pro- to anti-inflammatory mediators by neutrophils, platelets, and macrophages. PPARγand its ligands further modulate platelet and neutrophil function, decreasing trafficking, promoting neutrophil apoptosis, and preventing platelet-leukocyte interactions. PPARγalters macrophage trafficking, increases efferocytosis and phagocytosis, and promotes alternative M2 macrophage activation. There are also roles for this receptor in the adaptive immune response, particularly regarding B cells. These effects contribute towards the attenuation of multiple disease states, including COPD, colitis, Alzheimer’s disease, and obesity in animal models. Finally, novel specialized proresolving mediators—eicosanoids with critical roles in resolution—may act through PPARγmodulation to promote resolution, providing another exciting area of therapeutic potential for this receptor.

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Chen, Yituo, Haojie Zhang, Xinli Hu, Wanta Cai, Wenfei Ni, and Kailiang Zhou. "Role of NETosis in Central Nervous System Injury." Oxidative Medicine and Cellular Longevity 2022 (January 4, 2022): 1–15. http://dx.doi.org/10.1155/2022/3235524.

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Central nervous system (CNS) injury is divided into brain injury and spinal cord injury and remains the most common cause of morbidity and mortality worldwide. Previous reviews have defined numerous inflammatory cells involved in this process. In the human body, neutrophils comprise the largest numbers of myeloid leukocytes. Activated neutrophils release extracellular web-like DNA amended with antimicrobial proteins called neutrophil extracellular traps (NETs). The formation of NETs was demonstrated as a new method of cell death called NETosis. As the first line of defence against injury, neutrophils mediate a variety of adverse reactions in the early stage, and we consider that NETs may be the prominent mediators of CNS injury. Therefore, exploring the specific role of NETs in CNS injury may help us shed some light on early changes in the disease. Simultaneously, we discovered that there is a link between NETosis and other cell death pathways by browsing other research, which is helpful for us to establish crossroads between known cell death pathways. Currently, there is a large amount of research concerning NETosis in various diseases, but the role of NETosis in CNS injury remains unknown. Therefore, this review will introduce the role of NETosis in CNS injury, including traumatic brain injury, cerebral ischaemia, CNS infection, Alzheimer’s disease, and spinal cord injury, by describing the mechanism of NETosis, the evidence of NETosis in CNS injury, and the link between NETosis and other cell death pathways. Furthermore, we also discuss some agents that inhibit NETosis as therapies to alleviate the severity of CNS injury. NETosis may be a potential target for the treatment of CNS injury, so exploring NETosis provides a feasible therapeutic option for CNS injury in the future.

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Luo, Jiao, Jesper Qvist Thomassen, Børge G. Nordestgaard, Anne Tybjærg-Hansen, and Ruth Frikke-Schmidt. "Blood Leukocyte Counts in Alzheimer Disease." JAMA Network Open 5, no. 10 (October 10, 2022): e2235648. http://dx.doi.org/10.1001/jamanetworkopen.2022.35648.

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ImportanceEmerging evidence implicates a role for neuroinflammation in Alzheimer disease (AD) pathogenesis, predominantly involving the innate immune system. Blood leukocyte counts are easily accessible markers of immune function; however, their association with the risk of AD is unknown.ObjectiveTo investigate the observational and genetic associations between types of blood leukocytes and risk of AD.Design, Setting, and ParticipantsIn a cohort study comprising observational and genetic analyses, the Copenhagen General Population Study prospective cohort (n = 101 582) was used for the observational analyses. For the genetic studies, nonlinearity was first evaluated for the association between leukocyte cell counts and AD risk using individual-level data from the UK Biobank (n = 365 913). Subsequently, a 2-sample mendelian randomization framework was applied using genetic instruments for blood leukocyte counts (n = 563 085); for AD, the European Alzheimer &amp; Dementia Biobank was used, including 85 934 individuals with AD and 401 577 controls and the International Genomics of Alzheimer’s Project, including 21 982 individuals with AD and 41 944 controls.ExposuresObservational and genetically determined types of blood leukocyte counts.Main Outcomes and MeasuresHazard ratios (HRs) and 95% CIs for AD of cell count percentile groups in observational studies and odds ratios (ORs) and 95% CIs for AD per 1 SD genetically determined cell counts.ResultsThis cohort study included 101 582 participants (55 891 [55.0%] women) with a median age of 58 years (IQR, 48-67 years); of these, 1588 individuals developed AD. Multivariable-adjusted HRs for participants in the less than 5th vs the 25th to 75th (reference) percentile group were 1.24 (95% CI, 0.99-1.54) for blood monocytes and 1.25 for blood eosinophils (95% CI, 1.05-1.50). For participants in the greater than 95th vs the 25th to 75th percentile group, the HR was 1.30 (95% CI, 1.06-1.61) for blood neutrophils. Genetically, no evidence favored possible nonlinear associations. The ORs for AD per 1-SD decrease in genetically determined blood monocytes were 1.04 (95% CI, 1.00-1.10) in the European Alzheimer &amp; Dementia Biobank consortium and 1.09 (95% CI, 1.01-1.17) in the International Genomics of Alzheimer’s Project consortium. Using mendelian randomization, sensitivity analyses and multivariable analysis showed similar results.Conclusions and RelevanceThe findings of this study suggest that low blood monocyte counts are associated with increased AD risk. These findings highlight a potential role of the innate immune system in AD pathogenesis.

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Bracko, Oliver, Brendah N. Njiru, Madisen Swallow, Muhammad Ali, Mohammad Haft-Javaherian, and Chris B. Schaffer. "Increasing cerebral blood flow improves cognition into late stages in Alzheimer’s disease mice." Journal of Cerebral Blood Flow & Metabolism 40, no. 7 (September 7, 2019): 1441–52. http://dx.doi.org/10.1177/0271678x19873658.

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Alzheimer’s disease is associated with a 20–30% reduction in cerebral blood flow. In the APP/PS1 mouse model of Alzheimer’s disease, inhibiting neutrophil adhesion using an antibody against the neutrophil specific protein Ly6G was recently shown to drive rapid improvements in cerebral blood flow that was accompanied by an improvement in performance on short-term memory tasks. Here, in a longitudinal aging study, we assessed how far into disease development a single injection of anti-Ly6G treatment can acutely improve short-term memory function. We found that APP/PS1 mice as old as 15–16 months had improved performance on the object replacement and Y-maze tests of spatial and working short-term memory, measured at one day after anti-Ly6G treatment. APP/PS1 mice at 17–18 months of age or older did not show acute improvements in cognitive performance, although we did find that capillary stalls were still reduced and cerebral blood flow was still increased by 17% in 21–22-months-old APP/PS1 mice given anti-Ly6G antibody. These data add to the growing body of evidence suggesting that cerebral blood flow reductions are an important contributing factor to the cognitive dysfunction associated with neurodegenerative disease. Thus, interfering with neutrophil adhesion could be a new therapeutic approach for Alzheimer’s disease.

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Scali, Carla, Costanza Prosperi, Laura Bracco, Carolina Piccini, Roberto Baronti, Andrea Ginestroni, Sandro Sorbi, Giancarlo Pepeu, and Fiorella Casamenti. "Neutrophils CD11b and fibroblasts PGE2 are elevated in Alzheimer’s disease." Neurobiology of Aging 23, no. 4 (July 2002): 523–30. http://dx.doi.org/10.1016/s0197-4580(01)00346-3.

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Achilli, Cesare, Annarita Ciana, and Giampaolo Minetti. "Brain, immune system and selenium: a starting point for a new diagnostic marker for Alzheimer’s disease?" Perspectives in Public Health 138, no. 4 (May 29, 2018): 223–26. http://dx.doi.org/10.1177/1757913918778707.

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The clinical diagnosis of Alzheimer’s disease (AD) is based primarily on neuropsychological tests, which assess the involutive damage, and imaging techniques that evaluate morphologic changes in the brain. Currently available diagnostic tests do not show complete specificity and do not permit accurate differentiation between AD and other forms of senile dementia. The correlation of these tests with laboratory investigations based on biochemical parameters could increase the certainty of diagnosis. In recent years, several biochemical markers for the diagnosis of AD have been proposed, but in most cases they show a limited specificity and their application is invasive, requiring, in general, sampling of cerebrospinal fluid. Thus, the use of a peripheral biochemical marker could represent a valuable complement for the diagnosis of this disease. Several studies have shown a relationship between neurodegenerative disorders typical of the ageing process, weakening of the immune system and alterations in the levels of selenium and of the antioxidant selenoenzymes in brain tissues and blood cells. Among blood cells, neutrophil granulocytes uniquely express the selenoenzyme methionine sulfoxide reductase B1 (MsrB1). In a preliminary analysis carried out on neutrophils from subjects affected by AD, we observed a significant decline in MsrB1 activity compared to normal subjects. Therefore, we deem it of particular interest to explore the potential use of MsrB1 as a selective peripheral marker for the diagnosis of AD.

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Proskurnina, E. V., S. V. Sokolova, N. K. Grishina, M. M. Sozarukova, N. M. Gaifullin, and A. N. Khannanova. "The functional activity of neutrophils in paranoid schizophrenia and Alzheimer’s disease." Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova 120, no. 4 (2020): 97. http://dx.doi.org/10.17116/jnevro202012004197.

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Korbecki, Jan, Magdalena Gąssowska-Dobrowolska, Jerzy Wójcik, Iwona Szatkowska, Katarzyna Barczak, Mikołaj Chlubek, and Irena Baranowska-Bosiacka. "The Importance of CXCL1 in Physiology and Noncancerous Diseases of Bone, Bone Marrow, Muscle and the Nervous System." International Journal of Molecular Sciences 23, no. 8 (April 11, 2022): 4205. http://dx.doi.org/10.3390/ijms23084205.

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This review describes the role of CXCL1, a chemokine crucial in inflammation as a chemoattractant for neutrophils, in physiology and in selected major non-cancer diseases. Due to the vast amount of available information, we focus on the role CXCL1 plays in the physiology of bones, bone marrow, muscle and the nervous system. For this reason, we describe its effects on hematopoietic stem cells, myoblasts, oligodendrocyte progenitors and osteoclast precursors. We also present the involvement of CXCL1 in diseases of selected tissues and organs including Alzheimer’s disease, epilepsy, herpes simplex virus type 1 (HSV-1) encephalitis, ischemic stroke, major depression, multiple sclerosis, neuromyelitis optica, neuropathic pain, osteoporosis, prion diseases, rheumatoid arthritis, tick-borne encephalitis (TBE), traumatic spinal cord injury and West Nile fever.

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Baykan, Hayriye, Ozgur Baykan, Emre Cem Esen, Ayfer Tirak, Serap Akdeniz Gorgulu, and Tunay Karlidere. "Neutrophil-to-lymphocyte ratio as a potential differential diagnostic marker for Alzheimer’s disease, major depressive disorder, and Parkinson’s disease." Dusunen Adam: The Journal of Psychiatry and Neurological Sciences 31, no. 4 (December 26, 2018): 389–95. http://dx.doi.org/10.5350/dajpn2018310407.

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Kasus-Jacobi, Anne, Jennifer L. Washburn, Riley B. Laurence, and H. Anne Pereira. "Selecting Multitarget Peptides for Alzheimer’s Disease." Biomolecules 12, no. 10 (September 27, 2022): 1386. http://dx.doi.org/10.3390/biom12101386.

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Alzheimer’s disease (AD) is a multifactorial disease with a complex pathogenesis. Developing multitarget drugs could be a powerful strategy to impact the progressive loss of cognitive functions in this disease. The purpose of this study is to select a multitarget lead peptide candidate among a series of peptide variants derived from the neutrophil granule protein cathepsin G. We screened eight peptide candidates using the following criteria: (1) Inhibition and reversion of amyloid beta (Aβ) oligomers, quantified using an enzyme-linked immunosorbent assay (ELISA); (2) direct binding of peptide candidates to the human receptor for advanced glycation end-products (RAGE), the Toll-like receptor 4 (TLR4) and the S100 calcium-binding protein A9 (S100A9), quantified by ELISA; (3) protection against Aβ oligomer-induced neuronal cell death, using trypan blue to measure cell death in a murine neuronal cell line; (4) inhibition of TLR4 activation by S100A9, using a human TLR4 reporter cell line. We selected a 27-mer lead peptide that fulfilled these four criteria. This lead peptide is a privileged structure that displays inherent multitarget activity. This peptide is expected to significantly impact cognitive decline in mouse models of Alzheimer’s disease, by targeting both neuroinflammation and neurodegeneration.

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Ivanov, P. A., N. M. Mikhaylova, and T. P. Klyushnik. "Distribution of translation initiation factor eIF3 in neutrophils in Alzheimer disease." Biochemistry (Moscow) Supplement Series A: Membrane and Cell Biology 10, no. 4 (October 2016): 328–32. http://dx.doi.org/10.1134/s1990747816030053.

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Kuyumcu, Mehmet Emin, Yusuf Yesil, Zeynel Abidin Oztürk, Cemal Kizilarslanoglu, Sezgin Etgül, Meltem Halil, Zekeriya Ulger, Mustafa Cankurtaran, and Servet Ariogul. "The Evaluation of Neutrophil-Lymphocyte Ratio in Alzheimers Disease." Dementia and Geriatric Cognitive Disorders 34, no. 2 (2012): 69–74. http://dx.doi.org/10.1159/000341583.

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Serebrovska, Zoya O., Tetiana V. Serebrovska, Viktor A. Kholin, Lesya V. Tumanovska, Angela M. Shysh, Denis A. Pashevin, Sergii V. Goncharov, et al. "Intermittent Hypoxia-Hyperoxia Training Improves Cognitive Function and Decreases Circulating Biomarkers of Alzheimer’s Disease in Patients with Mild Cognitive Impairment: A Pilot Study." International Journal of Molecular Sciences 20, no. 21 (October 30, 2019): 5405. http://dx.doi.org/10.3390/ijms20215405.

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Alzheimer’s disease (AD) affects not only the central nervous system, but also peripheral blood cells including neutrophils and platelets, which actively participate in pathogenesis of AD through a vicious cycle between platelets aggregation and production of excessive amyloid beta (Aβ). Platelets adhesion on amyloid plaques also increases the risk of cerebral microcirculation disorders. Moreover, activated platelets release soluble adhesion molecules that cause migration, adhesion/activation of neutrophils and formation of neutrophil extracellular traps (NETs), which may damage blood brain barrier and destroy brain parenchyma. The present study examined the effects of intermittent hypoxic-hyperoxic training (IHHT) on elderly patients with mild cognitive impairment (MCI), a precursor of AD. Twenty-one participants (age 51–74 years) were divided into three groups: Healthy Control (n = 7), MCI+Sham (n = 6), and MCI+IHHT (n = 8). IHHT was carried out five times per week for three weeks (total 15 sessions). Each IHHT session consisted of four cycles of 5-min hypoxia (12% FIO2) and 3-min hyperoxia (33% FIO2). Cognitive parameters, Aβ and amyloid precursor protein (APP) expression, microRNA 29, and long non-coding RNA in isolated platelets as well as NETs in peripheral blood were investigated. We found an initial decline in cognitive function indices in both MCI+Sham and MCI+IHHT groups and significant correlations between cognitive test scores and the levels of circulating biomarkers of AD. Whereas sham training led to no change in these parameters, IHHT resulted in the improvement in cognitive test scores, along with significant increase in APP ratio and decrease in Aβ expression and NETs formation one day after the end of three-week IHHT. Such effects on Aβ expression and NETs formation remained more pronounced one month after IHHT. In conclusion, our results from this pilot study suggested a potential utility of IHHT as a new non-pharmacological therapy to improve cognitive function in pre-AD patients and slow down the development of AD.

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Fryer, John D., and Silvia S. Kang. "Translational profiling of microglia in Alzheimer’s disease models." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 166.56. http://dx.doi.org/10.4049/jimmunol.200.supp.166.56.

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Abstract Alzheimer’s disease (AD) is a neurodegenerative disease characterized pathologically by amyloidosis, tauopathy, and activation of microglia, the resident innate immune cells of the brain. Using a translational RiboTag profiling approach, we found that cellular isolation methods (enzymatic digestion, myelin removal, and CD45/CD11b sorting) altered the microglial transcriptome due to microglia activation and potential cellular contamination from sorting. Additionally, lipopolysaccharide-induced systemic inflammation generated completely different “top hits” from microglial RiboTag vs cellular isolation RNAseq datasets, likely due to microglial activation during the isolation process. RiboTag profiling of mouse models of AD revealed many significantly altered microglial transcripts that were shared between amyloidosis and tauopathy models, forming a network containing apolipoprotein E (APOE), CCL3, and CCL4. Inflammation and neutrophil chemotaxis pathways were also significantly enriched amongst the shared transcripts. This study has broad implications for microglial transcriptomic approaches and provides insights on microglial pathways associated with different pathological aspects of AD.

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Fulop, Tamas, Aurélie Y. Le Page, Eric H. Frost, and Gilles Dupuis. "Role of the innate immune response in the progression of Alzheimer’s disease." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 55.27. http://dx.doi.org/10.4049/jimmunol.198.supp.55.27.

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Abstract Alzheimer’s disease (AD) is a progressive irreversible neurological brain disorder. Inflammation and immune alterations have been linked to AD, suggesting that the peripheral immune system plays a role during the asymptomatic period of AD. NK cells and neutrophils (PMN) participate in innate immune surveillance against intracellular pathogens and malignancy but their role in AD remains controversial. We have investigated changes in peripheral NK cell and PMN phenotypes and functions in amnestic mild cognitive impairment (aMCI, n = 10), patients with mild AD (mAD, n = 11), and healthy elderly controls (n = 10). Patients selected according to NINCDS-ADRDA criteria were classified using neuropsychological assessment tests. Phenotype analysis revealed differences in expression of CD16 (increased in mAD), NKG2A (decreased in aMCI), and TLR2 and TLR9 (both decreased in mAD) for NK and CD14 (increased in MCI). Functional assays revealed that NK cell killing activity and degranulation (CD107 expression) were unchanged in the three groups. In contrast, expression of the CD95 receptor was increased in aMCI and mAD. Granzyme B expression and cytokine production (TNFα, IFNγ) were increased in aMCI but not in mAD. Similarly, PMN phagocytosis and free radical production were differentially modulated in MCI and mAD patients. Our data suggest that the number of alterations observed in peripheral NK cells and neutrophils in aMCI represent an activation state compared to mAD patients and that may reflect an active immune response against a still to be defined aggression.

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Sayed, Ahmed, Eshak I. Bahbah, Serageldin Kamel, George E. Barreto, Ghulam Md Ashraf, and Mohamed Elfil. "The neutrophil-to-lymphocyte ratio in Alzheimer's disease: Current understanding and potential applications." Journal of Neuroimmunology 349 (December 2020): 577398. http://dx.doi.org/10.1016/j.jneuroim.2020.577398.

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Gui, Huiwen, Qi Gong, Jun Jiang, Mei Liu, and Huanyin Li. "Identification of the Hub Genes in Alzheimer’s Disease." Computational and Mathematical Methods in Medicine 2021 (July 15, 2021): 1–8. http://dx.doi.org/10.1155/2021/6329041.

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Purpose. Alzheimer’s disease (AD) is considered to be the most common neurodegenerative disease and also one of the major fatal diseases affecting the elderly, thus bringing a huge burden to society. Therefore, identifying AD-related hub genes is extremely important for developing novel strategies against AD. Materials and Methods. Here, we extracted the gene expression profile GSE63061 from the National Center for Biotechnology Information (NCBI) GEO database. Once the unverified gene chip was removed, we standardized the microarray data after quality control. We utilized the Limma software package to screen the differentially expressed genes (DEGs). We conducted Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses of DEGs. Subsequently, we constructed a protein-protein interaction (PPI) network using the STRING database. Result. We screened 2169 DEGs, comprising 1313 DEGs with upregulation and 856 DEGs with downregulation. Functional enrichment analysis showed that the response of immune, the degranulation of neutrophils, lysosome, and the differentiation of osteoclast were greatly enriched in DEGs with upregulation; peptide biosynthetic process, translation, ribosome, and oxidative phosphorylation were dramatically enriched in DEGs with downregulation. 379 nodes and 1149 PPI edges were demonstrated in the PPI network constructed by upregulated DEGs; 202 nodes and 1963 PPI edges were shown in the PPI network constructed by downregulated DEGs. Four hub genes, including GAPDH, RHOA, RPS29, and RPS27A, were identified to be the newly produced candidates involved in AD pathology. Conclusion. GAPDH, RHOA, RPS29, and RPS27A are expected to be key candidates for AD progression. The results of this study can provide comprehensive insight into understanding AD’s pathogenesis and potential new therapeutic targets.

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Simi, A., N. Tsakiri, P. Wang, and N. J. Rothwell. "Interleukin-1 and inflammatory neurodegeneration." Biochemical Society Transactions 35, no. 5 (October 25, 2007): 1122–26. http://dx.doi.org/10.1042/bst0351122.

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Inflammation occurs rapidly in response to acute brain insults such as stroke, haemorrhage or trauma, and can be sustained for long periods of time, for example in Alzheimer's or Parkinson's diseases and multiple sclerosis. Experimental evidence indicates that inflammation plays a major role in neurodegeneration under these conditions, and that the cytokine IL-1 (interleukin-1) is a pivotal mediator. IL-1 is expressed rapidly in response to neuronal injury, predominantly by microglia, and elevated levels of endogenous or exogenous IL-1 markedly exacerbate injury. The naturally occurring IL-1RA (IL-1 receptor antagonist) markedly inhibits ischaemic, excitotoxic and traumatic brain injury in rodents, and has shown promise in a Phase II clinical trial in stroke patients. The mechanisms of IL-1 expression, release and action in neurodegeneration are not fully elucidated and appear multiple. Systemic IL-1 markedly enhances ischaemic brain injury via release of neutrophils into circulation, neutrophil adhesion to injured cerebrovasculature and CNS (central nervous system) invasion, and cell death via activation of matrix metalloproteinase-9. IL-1 also influences the release of toxins from glial and endothelial cells. Neuronal responses to excitotoxins and physiological factors may have an impact on neuronal survival. IL-1RA, delivered peripherally, can enter the CNS in animals and humans and has no adverse effects in stroke or subarachnoid haemorrhage patients, but shows potential benefit in acute stroke patients.

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Kim, Yeonjae, A. Yeon Cho, Hong Cheol Kim, Dajung Ryu, Sangmee Ahn Jo, and Yi-Sook Jung. "Effects of Natural Polyphenols on Oxidative Stress-Mediated Blood-Brain Barrier Dysfunction." Antioxidants 11, no. 2 (January 20, 2022): 197. http://dx.doi.org/10.3390/antiox11020197.

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The blood-brain barrier (BBB), which consists mainly of brain microvascular endothelial cells and astrocytes connected by tight junctions (TJs) and adhesion molecules (AMs), maintains the homeostatic balance between brain parenchyma and extracellular fluid. Accumulating evidence shows that BBB dysfunction is a common feature of neurodegenerative diseases, including stroke, traumatic brain injury, and Alzheimer’s disease. Among the various pathological pathways of BBB dysfunction, reactive oxygen species (ROS) are known to play a key role in inducing BBB disruption mediated via TJ modification, AM induction, cytoskeletal reorganization, and matrix metalloproteinase activation. Thus, antioxidants have been suggested to exert beneficial effects on BBB dysfunction-associated brain diseases. In this review, we summarized the sources of ROS production in multiple cells that constitute or surround the BBB, such as BBB endothelial cells, astrocytes, microglia, and neutrophils. We also reviewed various pathological mechanisms by which BBB disruption is caused by ROS in these cells. Finally, we summarized the effects of various natural polyphenols on BBB dysfunction to suggest a therapeutic strategy for BBB disruption-related brain diseases.

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Korte, Nils, Ross Nortley, and David Attwell. "Cerebral blood flow decrease as an early pathological mechanism in Alzheimer's disease." Acta Neuropathologica 140, no. 6 (August 31, 2020): 793–810. http://dx.doi.org/10.1007/s00401-020-02215-w.

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AbstractTherapies targeting late events in Alzheimer’s disease (AD), including aggregation of amyloid beta (Aβ) and hyperphosphorylated tau, have largely failed, probably because they are given after significant neuronal damage has occurred. Biomarkers suggest that the earliest event in AD is a decrease of cerebral blood flow (CBF). This is caused by constriction of capillaries by contractile pericytes, probably evoked by oligomeric Aβ. CBF is also reduced by neutrophil trapping in capillaries and clot formation, perhaps secondary to the capillary constriction. The fall in CBF potentiates neurodegeneration by upregulating the BACE1 enzyme that makes Aβ and by promoting tau hyperphosphorylation. Surprisingly, therefore, CBF reduction may play a crucial role in driving cognitive decline by initiating the amyloid cascade itself, or being caused by and amplifying Aβ production. Here, we review developments in this area that are neglected in current approaches to AD, with the aim of promoting novel mechanism-based therapeutic approaches.

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Sekhon, B. S., Saluja V, D. Chopra, and N. Singh. "Anti-inflammatory Potential of Dapsone Loaded Chitosan Nanoparticles in Streptozotocin-Induced Experimental Dementia." International Journal of Pharmaceutical Sciences and Nanotechnology 4, no. 1 (May 31, 2011): 1347–59. http://dx.doi.org/10.37285/ijpsn.2011.4.1.7.

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The potential of dapsone loaded characterized chitosan nanoparticles (CSNP) as a targeted delivery was investigated in memory deficits associated with dementia of Alzheimer disease type. Streptozotocin (STZ) in two doses (3 mg/kg on 1st and 3rd day) via intracerebroventricular route was used to induce dementia in swiss albino mice. The results showed that administration of STZ significantly impaired learning and memory based on Morris water-maze (MWM) test and raised myeloperoxidase (MPO) level along with neutrophils infiltration density (based on brain myeloperoxidase activity along with histological studies). Dapsone (1 mg/kg & 2 mg/kg for 11 days) loaded CSNP significantly attenuated STZ induced memory impairment as well as brain MPO activity along with increased neutrophils infiltration.

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Poon, Wayne, Anthony Carlos, Brittany Aguilar, and Carl Cotman. "P2-079: Neutrophin-trafficking deficits are mediated by impaired ubiquitin recycling in Alzheimer's disease." Alzheimer's & Dementia 8, no. 4S_Part_8 (July 2012): P291. http://dx.doi.org/10.1016/j.jalz.2012.05.783.

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Kalelioglu, Tevfik, Mehmet Yuruyen, Gozde Gultekin, Hakan Yavuzer, Yadigar Özturk, Meltem Kurt, Yildiray Topcu, Alper Doventas, and Murat Emul. "Neutrophil and platelet to lymphocyte ratios in people with subjective, mild cognitive impairment and early Alzheimer's disease." Psychogeriatrics 17, no. 6 (April 7, 2017): 506–8. http://dx.doi.org/10.1111/psyg.12260.

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Le Page, Aurélie, Julie Lamoureux, Karine Bourgade, Eric H. Frost, Graham Pawelec, Jacek M. Witkowski, Anis Larbi, Gilles Dupuis, and Tamàs Fülöp. "Polymorphonuclear Neutrophil Functions are Differentially Altered in Amnestic Mild Cognitive Impairment and Mild Alzheimer’s Disease Patients." Journal of Alzheimer's Disease 60, no. 1 (August 29, 2017): 23–42. http://dx.doi.org/10.3233/jad-170124.

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Apostolova, Elisaveta, Paolina Lukova, Alexandra Baldzhieva, Plamen Katsarov, Mariana Nikolova, Ilia Iliev, Lyudmil Peychev, et al. "Immunomodulatory and Anti-Inflammatory Effects of Fucoidan: A Review." Polymers 12, no. 10 (October 13, 2020): 2338. http://dx.doi.org/10.3390/polym12102338.

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Inflammation is the initial response of the immune system to potentially harmful stimuli (e.g., injury, stress, and infections). The process involves activation of macrophages and neutrophils, which produce mediators, such as nitric oxide (NO), prostaglandin E2 (PGE2), pro-inflammatory and anti-inflammatory cytokines. The pro-inflammatory cytokines interleukin-1β (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor-α (TNF-α) are considered as biomarkers of inflammation. Even though it occurs as a physiological defense mechanism, its involvement in the pathogenesis of various diseases is reported. Rheumatoid arthritis, inflammatory bowel disease, Alzheimer’s disease, and cardiovascular diseases are only a part of the diseases, in which pathogenesis the chronic inflammation is involved. Fucoidans are complex polysaccharides from brown seaweeds and some marine invertebrates, composed mainly of l-fucose and sulfate ester groups and minor amounts of neutral monosaccharides and uronic acids. Algae-derived fucoidans are studied intensively during the last years regarding their multiple biological activities and possible therapeutic potential. However, the source, species, molecular weight, composition, and structure of the polysaccharides, as well as the route of administration of fucoidans, could be crucial for their effects. Fucoidan is reported to act on different stages of the inflammatory process: (i) blocking of lymphocyte adhesion and invasion, (ii) inhibition of multiple enzymes, and (iii) induction of apoptosis. In this review, we focused on the immunemodulating and anti-inflammatory effects of fucoidans derived from macroalgae and the models used for their evaluation. Additional insights on the molecular structure of the compound are included.

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Dong, Yeqing, Tongxin Li, Zhonghui Ma, Chi Zhou, Xinxu Wang, and Jie Li. "HSPA1A, HSPA2, and HSPA8 Are Potential Molecular Biomarkers for Prognosis among HSP70 Family in Alzheimer’s Disease." Disease Markers 2022 (September 30, 2022): 1–16. http://dx.doi.org/10.1155/2022/9480398.

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Alzheimer’s disease (AD) is a chronic neurodegenerative disease, which leads to impairment of cognition and memory. The heat shock protein 70 (HSP70) family plays an important role in the pathogenesis of AD. It is known to regulate protein misfolding in a variety of diseases, including inhibition of Aβ aggregation and NFT formation in AD. As yet, the diagnostic molecular markers of AD remain unclear. Herein, we sought to investigate molecular markers of HSP70 family that can affect diagnosis and treatment in AD through computational analysis. In this study, the intersection between HSP70 family members and immune molecules was taken to screen immune-related HSP70 family genes. Based on the datasets from the NCBI-Gene Expression Omnibus (GEO) database, we found that the expression levels of HSPA1A and HSPA2 were significantly increased in AD samples, while HSPA8 significantly decreased. Surprisingly, the combination of the 3 hub genes had a good diagnosis of AD via receiver operating characteristic curve (ROC). Moreover, the clinical value of the 3 hub genes was further assessed by the Spearman correlation analysis with AD-related genes, β-secretase activity, and γ-secretase activity. In terms of immune cell infiltration, we showed that the distribution of seven immune cell types (macrophages M2, neutrophils, T cells CD4 memory activated, macrophages M0, NK cells activated, plasma cells, and T cells follicular helper) was associated with the occurrence of AD by CIBERSORT. Furthermore, our data suggested that EP300, MYC, TP53, JUN, CREBBP, and ESR1 might be key transcription factors (TFs) for the 3 hub genes. In general, these findings suggest that HSPA1A, HSPA2, and HSPA8 are potential molecular biomarkers for prognosis among HSP70 family in AD, and it provides a new perspective on diagnostic and therapeutic targets for AD.

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Cahilog, Zhen, Hailin Zhao, Lingzhi Wu, Azeem Alam, Shiori Eguchi, Hao Weng, and Daqing Ma. "The Role of Neutrophil NETosis in Organ Injury: Novel Inflammatory Cell Death Mechanisms." Inflammation 43, no. 6 (August 24, 2020): 2021–32. http://dx.doi.org/10.1007/s10753-020-01294-x.

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Abstract NETosis is a type of regulated cell death dependent on the formation of neutrophil extracellular traps (NET), where net-like structures of decondensed chromatin and proteases are produced by polymorphonuclear (PMN) granulocytes. These structures immobilise pathogens and restrict them with antimicrobial molecules, thus preventing their spread. Whilst NETs possess a fundamental anti-microbial function within the innate immune system under physiological circumstances, increasing evidence also indicates that NETosis occurs in the pathogenic process of other disease type, including but not limited to atherosclerosis, airway inflammation, Alzheimer’s and stroke. Here, we reviewed the role of NETosis in the development of organ injury, including injury to the brain, lung, heart, kidney, musculoskeletal system, gut and reproductive system, whilst therapeutic agents in blocking injuries induced by NETosis in its primitive stages were also discussed. This review provides novel insights into the involvement of NETosis in different organ injuries, and whilst potential therapeutic measures targeting NETosis remain a largely unexplored area, these warrant further investigation.

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Rembach, Alan, Bill Wilson, Kathryn Ellis, David Ames, Christopher Rowe, Victor Villemagne, Ashley Bush, Ralph Martins, Colin Masters, and James Doecke. "P1-146: Neutrophil-lymphocyte ratio in Alzheimer's disease: Data from the Australian Imaging Biomarker and Lifestyle study of ageing." Alzheimer's & Dementia 9 (July 2013): P203. http://dx.doi.org/10.1016/j.jalz.2013.05.368.

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Sulik, Artur, Kacper Toczylowski, Agnieszka Kulczynska-Przybik, and Barbara Mroczko. "Amyloid and Tau Protein Concentrations in Children with Meningitis and Encephalitis." Viruses 14, no. 4 (March 30, 2022): 725. http://dx.doi.org/10.3390/v14040725.

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Alzheimer’s disease (AD) has emerged as a growing threat to human health. It is a multifactorial disorder, in which abnormal amyloid beta metabolism and neuroinflammation have been demonstrated to play a key role. Intrathecal inflammation can be triggered by infections and precede brain damage for years. We analyzed the influence of infections of the central nervous system on biomarkers that are crucially involved in AD pathology. Analyses of the cerebrospinal fluid (CSF) levels of Aβ1–42, Aβ1–40, Tau, and pTau proteins were performed in 53 children with neuroinfections of viral (n = 26) and bacterial origin (n = 19), and in controls (n = 8). We found no changes in CSF amyloid Aβ1–42 concentrations, regardless of etiology. We showed an increase in tau and phosphorylated tau concentrations in purulent CNS infections of the brain, compared to other etiologies. Moreover, the total concentrations of tau in the CSF correlated with the CSF absolute number of neutrophils. These findings and the Aβ 42/40 concentration quotient discrepancies in CFS between meningitis and encephalitis suggest that infections may affect the metabolism of AD biomarkers.

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Della Bianca, Vittorina, Elena Zenaro, Gennj Piacentino, Enrica Caterina Pietronigro, Silvia Dusi, Tommaso Carlucci, Carlo Laudanna, and Gabriela Constantin. "P3-113: LFA-1 Integrin Mediates Neutrophil Trafficking in the Brain And Contributes to Disease Pathology in Mouse Models of Alzheimer’s Disease." Alzheimer's & Dementia 12 (July 2016): P862. http://dx.doi.org/10.1016/j.jalz.2016.06.1771.

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Benayoun, Bérénice. "SEX DIMORPHISM IN AGING." Innovation in Aging 6, Supplement_1 (November 1, 2022): 164–65. http://dx.doi.org/10.1093/geroni/igac059.656.

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Abstract In this symposium, the speakers will discuss how sex can influence aging trajectories using complementary perspectives and approaches across multiple biological scales and systems. Indeed, accumulating evidence across species has revealed that aging is a highly sex-dimorphic process. On the one hand, women outlive men consistently across populations, and most supercentanarians are women. On the other hand, especially after the onset of menopause, women are at increased risk for most age-related diseases (e.g. Alzheimer’s disease, osteoporosis, etc.). However, the molecular pathways underlying such sex-differences in aging and longevity are still largely unexplored and poorly understood. Dr. Austad will discuss how compatibility between the mitochondrial and nuclear genomes during aging is influenced as a function of sex. Dr. Dubal will discuss the impact of sex chromosome complement on cognition with aging in mouse models, and how sex chromosomes may underlie sex-differences in brain aging. Dr. Ucar will discuss work from her lab revealing that the genomic signatures of immune aging in humans are specific to sex. Finally, Dr. Benayoun will discuss how aging of innate immune cells (e.g. macrophages or neutrophils) is regulated by the female vs. male milieu, with sex-specific age-related trajectories remodeling the immune compartment in mice.

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Cruz Hernández, Jean C., Oliver Bracko, Calvin J. Kersbergen, Victorine Muse, Mohammad Haft-Javaherian, Maxime Berg, Laibaik Park, et al. "Neutrophil adhesion in brain capillaries reduces cortical blood flow and impairs memory function in Alzheimer’s disease mouse models." Nature Neuroscience 22, no. 3 (February 11, 2019): 413–20. http://dx.doi.org/10.1038/s41593-018-0329-4.

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Khalil, Faiza, Noreen Samad, Sohaib Hassan, Muhammad Ali Qureshi, and Ahsan Numan. "Hematological Profile of Patients with Dementia in South Punjab." Pakistan Journal Of Neurological Surgery 25, no. 2 (June 14, 2021): 156–64. http://dx.doi.org/10.36552/pjns.v25i2.538.

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Objectives: A case-control study was conducted to find the prevalence of abnormal blood indices and electrolytes in patients with dementia. Material & Methods: The levels of erythrocytes, leukocytes, platelets, electrolytes, and ESR were determined from the biochemistry lab. A t-test was applied to see the significance of the difference between each dementia patient group (Alzheimer Disease-AD, Parkinson’s Disease-PD, and Frontotemporal Dementia-FTD) with the control group for each CBC and electrolyte parameter Results: In each patients’ groups (AD, PD, and FTD), the mean value of every erythrocyte was lower than the normal range. A significant difference existed for each erythrocyte between dementia patients and controls, except MCHC. Low levels were observed in neutrophils in all groups of dementia including control group. Very high levels were observed in ESR in all groups of dementia. Significant differences existed in the WBC levels between controls and AD as well as PD patients, in platelets between the control group and FTD patients, and in ESR in each group of dementia patients vs. control group. Normal values observed in all groups of dementia patients as well as in the control group. Conclusion: We found low levels in erythrocytes in cases of Alzheimer disease, Parkinson’s disease, and frontotemporal dementia. Age-related changes to hematological indices especially related to RBCs, and inflammatory mediators like cytokines, hamper the microcirculation in the cerebral tissue leading to micro-infarcts or microbleeds which cause neuronal insults and parenchymal damage.

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Li, Qingqin S., Chao Tian, David Hinds, and Guy R. Seabrook. "The association of clinical phenotypes to known AD/FTD genetic risk loci and their inter-relationship." PLOS ONE 15, no. 11 (November 5, 2020): e0241552. http://dx.doi.org/10.1371/journal.pone.0241552.

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To elucidate how variants in genetic risk loci previously implicated in Alzheimer’s Disease (AD) and/or frontotemporal dementia (FTD) contribute to expression of disease phenotypes, a phenome-wide association study was performed in two waves. In the first wave, we explored clinical traits associated with thirteen genetic variants previously reported to be linked to disease risk using both the 23andMe and UKB cohorts. We tested 30 additional AD variants in UKB cohort only in the second wave. APOE variants defining ε2/ε3/ε4 alleles and rs646776 were identified to be significantly associated with metabolic/cardiovascular and longevity traits. APOE variants were also significantly associated with neurological traits. ABI3 variant rs28394864 was significantly associated with cardiovascular (e.g. (hypertension, ischemic heart disease, coronary atherosclerosis, angina) and immune-related trait asthma. Both APOE variants and CLU variant were significantly associated with nearsightedness. HLA- DRB1 variant was associated with diseases with immune-related traits. Additionally, variants from 10+ AD genes (BZRAP1-AS1, ADAMTS4, ADAM10, APH1B, SCIMP, ABI3, SPPL2A, ZNF232, GRN, CD2AP, and CD33) were associated with hematological measurements such as white blood cell (leukocyte) count, monocyte count, neutrophill count, platelet count, and/or mean platelet (thrombocyte) volume (an autoimmune disease biomarker). Many of these genes are expressed specifically in microglia. The associations of ABI3 variant with cardiovascular and immune-related traits are one of the novel findings from this study. Taken together, it is evidenced that at least some AD and FTD variants are associated with multiple clinical phenotypes and not just dementia. These findings were discussed in the context of causal relationship versus pleiotropy via Mendelian randomization analysis.

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Rembach, Alan, Andrew D. Watt, William J. Wilson, Stephanie Rainey-Smith, Kathryn A. Ellis, Christopher C. Rowe, Victor L. Villemagne, et al. "An increased neutrophil–lymphocyte ratio in Alzheimer's disease is a function of age and is weakly correlated with neocortical amyloid accumulation." Journal of Neuroimmunology 273, no. 1-2 (August 2014): 65–71. http://dx.doi.org/10.1016/j.jneuroim.2014.05.005.

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Constantin, Gabriela, Elena Zenaro, Stefano Angiari, Enrica Caterina Pietronigro, Vittorina Della Bianca, Rajasekar Nagarajan, Gennj Piacentino, Jessica Arioli, Giulia Iannoto, and Marco Bonani. "TIM-1 CONTROLS NEUTROPHIL TRAFFICKING AND CONTRIBUTES TO THE INDUCTION OF COGNITIVE DECLINE AND NEUROPATHOLOGICAL CHANGES IN ANIMAL MODELS OF ALZHEIMER'S DISEASE." Alzheimer's & Dementia 13, no. 7 (July 2017): P228. http://dx.doi.org/10.1016/j.jalz.2017.07.113.

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Journal articles on the topic 'Neutrophils, Alzheimer's disease'

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