Abstract

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.

Keywords

MicrogliaInflammationNeurosciencePathogenesisNeuroinflammationMechanism (biology)DiseaseImmune systemAmyloid (mycology)Cognitive declineAlzheimer's diseaseMedicineImmunologyBiologyDementiaPathology

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Publication Info

Year
2018
Type
review
Volume
4
Issue
1
Pages
575-590
Citations
2108
Access
Closed

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Jefferson W. Kinney, Shane M. Bemiller, Andrew S. Murtishaw et al. (2018). Inflammation as a central mechanism in Alzheimer's disease. Alzheimer s & Dementia Translational Research & Clinical Interventions , 4 (1) , 575-590. https://doi.org/10.1016/j.trci.2018.06.014

Identifiers

DOI
10.1016/j.trci.2018.06.014
PMID
30406177
PMCID
PMC6214864

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Data completeness: 86%