Relevant bibliographies by topics / Neutrophils, Alzheimer's disease

Academic literature on the topic 'Neutrophils, Alzheimer's disease'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "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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Dissertations / Theses on the topic "Neutrophils, Alzheimer's disease"

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Dong, Yuan. "Implication des polynucléaires neutrophiles au cours de la maladie d’Alzheimer et des tauopathies Neutrophil hyperactivation correlates with Alzheimer's disease progression Reduced Oxidative Burst by Primed Neutrophils in the Elderly Individuals Is Associated With Increased Levels of the CD16bright/CD62Ldim Immunosuppressive Subset." Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS445.

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Les Polynucléaires neutrophiles (PN) jouent un rôle majeur dans la défense de l’organisme contre l’introduction d’un agent pathogène. Cependant, les PN peuvent également conduire à des lésions tissulaires majeures et être impliqués dans la physiopathologie de nombreuses maladies inflammatoires. Nous avons observé, dans une cohorte des patients atteints maladie d’Alzheimer (MA) au stade de démence, une hyper-activation basale des PN, associée à une augmentation de la production des formes réactives d’oxygène (FRO) et des NETs. Les PN circulants chez les patients de la MA présentent également une altération de l’homéostasie associée à une augmentation de la population sénescente CXCR4high/CD62Llow et une diminution de la population immunosuppressive CD16bright/CD62Ldim. Ces altérations qui sont plus importantes chez les patients dont la progression de la maladie est rapide pourraient contribuer au déclin cognitif. Par ailleurs, certaines anomalies, notamment l’augmentation de la production de FRO et la diminution de la population de PN immunosuppressive, ont été observées chez les patients atteints de MA atypiques mais ne sont pas retrouvées en cas de tauopathies, Elles apparaissent donc spécifiques de la pathologie amyloïde. Le phénotype des PN pourrait donc représenter un bio-marqueur prédictif sanguin innovant en cas de pathologie amyloïde. Par ailleurs, nos résultats ouvrent de nouvelles perspectives pour le développement de nouvelles stratégies d’immunothérapie au cours de la MA basées sur la modulation des PN
Neutrophils are key components of early innate immunity and contribute to uncontrolled systemic inflammation if not tightly regulated. Our study demonstrated that blood samples from Alzheimer’s Disease (AD) patients with dementia revealed neutrophil hyperactivation associated with increased reactive oxygen species (ROS) production and increased levels of intravascular neutrophil extravascular traps. The homeostasis of circulating neutrophils in these patients also changed: the ratio between the harmful hyperreactive CXCR4high/CD62Llow senescent and the CD16bright/CD62Ldim immunosuppressive neutrophil subsets rose in the latter stage of the disease. These abnormalities, that may play an instrumental role in establishing systemic chronic inflammation, were greater in fast-decliner than in slow-decliner patients. Some abnormalities, including the increased level of ROS production, were observed in patients with atypic AD but not in Tauopathies suggesting that these alterations are specific of amyloid pathology. Our data strongly suggest that the neutrophil phenotype may constitute an innovative and prognostic blood biomarker in patients with Alzheimer’s disease open new perspectives for the development of innovative immunotherapy strategies based on neutrophil modulation
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Book chapters on the topic "Neutrophils, Alzheimer's disease"

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Harding, Alice, Sarita Robinson, StJohn Crean, and Sim K. Singhrao. "Can Better Management of Periodontal Disease Delay the Onset and Progression of Alzheimer’s Disease?" In Advances in Alzheimer’s Disease. IOS Press, 2022. http://dx.doi.org/10.3233/aiad220040.

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A risk factor relationship exists between periodontal disease and Alzheimer’s disease (AD) via tooth loss, and improved memory following dental intervention. This links the microbial contribution from indigenous oral periodontal pathogens to the manifestation of chronic conditions, such as AD. Here, we use Porphyromonas gingivalis infection to illustrate its effect on mental health. P. gingivalis infection, in its primary sub-gingival niche, can cause polymicrobial synergy and dysbiosis. Dysbiosis describes the residency of select commensals from the oral cavity following co-aggregation around the dominant keystone pathogen, such as P. gingivalis, to gain greater virulence. The initial process involves P. gingivalis disturbing neutrophil mediated innate immune responses in the healthy gingivae and then downregulating adaptive immune cell differentiation and development to invade, and subsequently, establish new dysbiotic bacterial communities. Immune responses affect the host in general and functionally via dietary adjustments caused by tooth loss. Studies from animals orally infected with P. gingivalis confirm this bacterium can transmigrate to distant organ sites (the brain) and contribute toward peripheral and intracerebral inflammation, and compromise vascular and microvascular integrity. In another study, P. gingivalis infection caused sleep pattern disturbances by altering glial cell light/dark molecular clock activity, and this, in turn, can affect the clearance of danger associated molecular patterns, such as amyloid-β, via the glymphatic system. Since P. gingivalis can transmigrate to the brain and modulate organ-specific inflammatory innate and adaptive immune responses, this paper explores whether better management of indigenous periodontal bacteria could delay/prevent the onset and/or progression of dementia.
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Conference papers on the topic "Neutrophils, Alzheimer's disease"

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Gomes, Karina, Maria Carvalho, Ramon Pereira, Henrique Guimarães, Antônio Teixeira, Alexandre Braga, Maira Barbosa, Wagner Junior, and Paulo Caramelli. "MACHINE LEARNING-BASED ROUTINE LABORATORY VARIABLES SCREENING FOR ONE-YEAR COGNITIVE AND FUNCTIONAL DECLINE IN INDIVIDUALS AGED 75+ YEARS: THE PIETÀ STUDY." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda004.

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Background: Cognitive and functional decline are important health problems in older adults. Objectives: To investigate Machine Learning (ML) algorithms of routine laboratory variables in predicting cognitive and functional decline in a population-based sample aged 75+ years within one-year. Methods: 132 individuals were selected from a population-based project. Functional and cognitive performances were evaluated at baseline and one year after. Results of routine laboratory tests obtained at baseline were used to generate three ML algorithms. Results: Random forest (RF), including triglycerides, glucose, hematocrit, RDW, albumin, hemoglobin, globulin, HDL, TSH, creatinine, lymphocyte, erythrocyte, platelet/leucocyte (PLR) and neutrophil/leucocyte (NLR) ratios, ALT, leukocyte, LDL, cortisol, GGT and eosinophil, showed the best performance to predict the cognitive decline (accuracy = 0.80). For functional decline (accuracy =0.92), the most important RF variables were platelet, PLR and NLR, hemoglobin, globulin, cortisol, RDW, glucose, basophil, B12 vitamin, creatinine, GGT, ALT, AST, eosinophil, hematocrit, erythrocyte, triglycerides, HDL and monocyte. Conclusions: Our results suggest that ML presents a good accuracy to predict cognitive and functional decline in oldest-old subjects using routine laboratory variables.
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Eberhart, Robert C. "Reflections on Quantitative Gamma Imaging of Cell-Surface Interactions." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53388.

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Molecular and cellular interactions with foreign surfaces can be noninvasively measured by isotope imaging techniques. Long available for probing cell behavior, these techniques are now employed in molecular studies of disease progression, such as Alzheimer’s [1]. This paper reviews results obtained by noninvasive dual label gamma scintigraphy for the transient adhesion of platelets and neutrophils to pump-oxygenators during cardiopulmonary bypass (CPB). In this application, characteristic cell-foreign surface adhesion and release patterns are observed during CPB in the pig, as a function of oxygenator design and surface chemistry. Cell distributions in internal organs post-CPB are also affected by these processes. This method can be adapted to other settings where the understanding of protein-cell interactions with native and foreign surfaces is at issue, including fibrinogen-cell interactions, bacterial colonization, etc.
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Poxleitner, M., SH Hoffmann, A. Maurer, G. Reischl, AM Wild, CM Griessinger, S. Wiehr, BJ Pichler, and FC Maier. "Dual in vivo PET ex vivo FACS cell tracking of neutrophils – first results in a mouse model of Alzheimer disease." In NuklearMedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1683636.

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