Alzheimer s & Dementia Translational Research & Clinical Interventions· 2018Q1· Review
Inflammation as a central mechanism in Alzheimer's disease
- 2,269citations
- Q1SCImago
- 2018year
Short summary
Inflammation, driven by sustained activation of brain immune cells like microglia, is now recognized as a third core pathology in Alzheimer's disease (AD), exacerbating amyloid and tau pathologies.
AI-generated from the title and abstract; the full text is not read.
Key points
- Inflammation is identified as a third core pathology in Alzheimer's disease.
- Sustained activation of microglia and other brain immune cells drives AD inflammation.
- This immune response exacerbates amyloid β plaques and neurofibrillary tangles.
- Microglia signaling pathways and cytokines are key implicated mechanisms.
AI-generated from the title and abstract; the full text is not read.
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized by cognitive decline and the presence of two core pathologies, amyloid β plaques and neurofibrillary tangles. Over the last decade, the presence of a sustained immune response in the brain has emerged as a third core pathology in AD. The sustained activation of the brain's resident macrophages (microglia) and other immune cells has been demonstrated to exacerbate both amyloid and tau pathology and may serve as a link in the pathogenesis of the disorder. In the following review, we provide an overview of inflammation in AD and a detailed coverage of a number of microglia-related signaling mechanisms that have been implicated in AD. Additional information on microglia signaling and a number of cytokines in AD are also reviewed. We also review the potential connection of risk factors for AD and how they may be related to inflammatory mechanisms.
The authors' abstract, as published at the source. Alzheimer s & Dementia Translational Research & Clinical Interventions, 2018 · DOI ↗
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Field: Neurology (Neuroscience)
NeurologyNeuroscience