Alzheimer's disease

The Lancet, Год журнала: 2021, Номер 397(10284), С. 1577 - 1590

Опубликована: Март 2, 2021

Язык: Английский

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Inflammation in obesity, diabetes, and related disorders

Immunity, Год журнала: 2022, Номер 55(1), С. 31 - 55

Опубликована: Янв. 1, 2022

Язык: Английский

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Spatial Transcriptomics and In Situ Sequencing to Study Alzheimer’s Disease

Cell, Год журнала: 2020, Номер 182(4), С. 976 - 991.e19

Опубликована: Июль 22, 2020

Язык: Английский

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Role of neuroinflammation in neurodegeneration development

Signal Transduction and Targeted Therapy, Год журнала: 2023, Номер 8(1)

Опубликована: Июль 12, 2023

Abstract Studies in neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease and Amyotrophic lateral sclerosis, Huntington’s so on, have suggested that inflammation is not only a result of neurodegeneration but also crucial player this process. Protein aggregates which are very common pathological phenomenon can induce neuroinflammation further aggravates protein aggregation neurodegeneration. Actually, even happens earlier than aggregation. Neuroinflammation induced by genetic variations CNS cells or peripheral immune may deposition some susceptible population. Numerous signaling pathways range been to be involved the pathogenesis neurodegeneration, although they still far from being completely understood. Due limited success traditional treatment methods, blocking enhancing inflammatory considered promising strategies for therapy many them got exciting results animal models clinical trials. Some them, few, approved FDA usage. Here we comprehensively review factors affecting major pathogenicity sclerosis. We summarize current strategies, both clinic, diseases.

Язык: Английский

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Microglia Polarization From M1 to M2 in Neurodegenerative Diseases

Frontiers in Aging Neuroscience, Год журнала: 2022, Номер 14

Опубликована: Фев. 16, 2022

Microglia-mediated neuroinflammation is a common feature of neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's (PD), amyotrophic lateral sclerosis (ALS), and multiple (MS). Microglia can be categorized into two opposite types: classical (M1) or alternative (M2), though there's continuum different intermediate phenotypes between M1 M2, microglia transit from one phenotype to another. release inflammatory mediators induce inflammation neurotoxicity, while M2 anti-inflammatory neuroprotectivity. considered double-edged sword, performing both harmful helpful effects in diseases. Previous studies showed that balancing M1/M2 polarization had promising therapeutic prospect We suggest shifting may significant we focus on the modulation especially by important signal pathways,

Язык: Английский

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The semantics of microglia activation: neuroinflammation, homeostasis, and stress

Journal of Neuroinflammation, Год журнала: 2021, Номер 18(1)

Опубликована: Ноя. 6, 2021

Microglia are emerging as critical regulators of neuronal function and behavior in nearly every area neuroscience. Initial reports focused on classical immune functions microglia pathological contexts, however, immunological concepts from these studies have been applied to describe neuro-immune interactions the absence disease, injury, or infection. Indeed, terms such 'microglia activation' 'neuroinflammation' used ubiquitously changes disparate contexts; particularly stress research, where prompt undue comparisons conditions. This creates a barrier for investigators new neuro-immunology ultimately hinders our understanding effects microglia. As more seek understand role neurobiology behavior, it is increasingly important develop standard methods study define microglial phenotype function. In this review, we summarize primary research physiological contexts. Further, propose framework better microglia1 chronic stress. approach will enable precise characterization different which should facilitate development microglia-directed therapeutics psychiatric neurological disease.

Язык: Английский

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Amyloid-β-independent regulators of tau pathology in Alzheimer disease

Nature reviews. Neuroscience, Год журнала: 2019, Номер 21(1), С. 21 - 35

Опубликована: Ноя. 28, 2019

Язык: Английский

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Alzheimer's disease: Recent treatment strategies

European Journal of Pharmacology, Год журнала: 2020, Номер 887, С. 173554 - 173554

Опубликована: Сен. 14, 2020

Язык: Английский

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The Physiology, Pathology, and Potential Therapeutic Applications of the TREM2 Signaling Pathway

Cell, Год журнала: 2020, Номер 181(6), С. 1207 - 1217

Опубликована: Июнь 1, 2020

Язык: Английский

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Type I interferon response drives neuroinflammation and synapse loss in Alzheimer disease

Journal of Clinical Investigation, Год журнала: 2020, Номер 130(4), С. 1912 - 1930

Опубликована: Янв. 9, 2020

Type I interferon (IFN) is a key cytokine that curbs viral infection and cell malignancy. Previously, we demonstrated potent IFN immunogenicity of nucleic acid–containing (NA-containing) amyloid fibrils in the periphery. Here, investigated whether associated with β-amyloidosis inside brain contributes to neuropathology. An IFN-stimulated gene (ISG) signature was detected brains multiple murine Alzheimer disease (AD) models, phenomenon also observed WT mouse challenged generic NA-containing fibrils. In vitro, microglia innately responded AD activated ISG-expressing exclusively surrounded NA+ β plaques, which accumulated an age-dependent manner. Brain administration rIFN-β resulted microglial activation complement C3-dependent synapse elimination vivo. Conversely, selective receptor blockade effectively diminished ongoing microgliosis loss models. Moreover, enveloping neuritic plaques postmortem patients AD. Gene expression interrogation revealed pathway grossly upregulated clinical significantly correlated severity activation. Therefore, constitutes pivotal element within neuroinflammatory network critically neuropathogenic processes.

Язык: Английский

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