Cyclical amyloid beta-astrocyte activity induces oxidative stress in Alzheimer’s disease

Glial cell involvement in Alzheimer’s disease (AD) is multi-faceted. The role of astrocytes in AD pathology, both as a causative agent of amyloid-beta (Aβ) production as well as a casualty of dysfunction resulting from the presence of Aβ has been well-delineated. In this review, we explore the influ...

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Bibliographic Details
Published in:Biochimie 2020-04, Vol.171-172, p.38-42
Main Authors: Elangovan, Shalini, Holsinger, R.M. Damian
Format: Article
Language:English
Subjects:
Alzheimer Disease - metabolism
Alzheimer Disease - pathology
Amyloid beta-Peptides - metabolism
Animals
Astrocytes - metabolism
Astrocytes - pathology
Brain - metabolism
Brain - pathology
Calcium - metabolism
Calcium dyshomeostasis
Calcium oscillations
Cytokines - metabolism
Glial cells
Humans
Mice
Microglia - metabolism
NADPH Oxidases - metabolism
Oxidative Stress
Reactive nitrogen species (RNS)
Reactive Nitrogen Species - metabolism
Reactive oxygen species (ROS)
Reactive Oxygen Species - metabolism
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Summary:Glial cell involvement in Alzheimer’s disease (AD) is multi-faceted. The role of astrocytes in AD pathology, both as a causative agent of amyloid-beta (Aβ) production as well as a casualty of dysfunction resulting from the presence of Aβ has been well-delineated. In this review, we explore the influence of oxidative stress in astrocytes and the subsequent effect on Aβ levels in the brain from a perspective of intracellular calcium homeostasis and NADPH oxidase activity. The response of astrocytes to the presence of Aβ, as well astrocytic and microglial interaction and inflammatory cytokine release is also discussed, highlighting a cyclical behaviour of these cells in contributing to AD pathogenesis. •Aβ induces Ca2+ oscillation dyshomeostasis and oxidative stress in astrocytes, perturbing normal astrocytic function.•NOX activation results in ROS production and increased neurotoxicity.•Interaction of astrocytes with amyloid plaques warps the protective mechanisms ascribed to these cells.•Pro-inflammatory cytokines are key mediators in the transformation of astrocytes from ‘protectors’ to ‘culprits’.•Dampening neuroinflammation may be key to mitigating astrocytic transformation and represents a therapeutic avenue for AD.
ISSN:0300-9084
1638-6183
DOI:10.1016/j.biochi.2020.02.003