Microglia and the aging brain: are senescent microglia the key to neurodegeneration?

Dafina M. Angelova, David R. Brown

Research output: Contribution to journalReview articlepeer-review

177 Citations (SciVal)
160 Downloads (Pure)

Abstract

The single largest risk factor for etiology of neurodegenerative diseases like Alzheimer's disease is increased age. Therefore, understanding the changes that occur as a result of aging is central to any possible prevention or cure for such conditions. Microglia, the resident brain glial population most associated with both protection of neurons in health and their destruction is disease, could be a significant player in age related changes. Microglia can adopt an aberrant phenotype sometimes referred to either as dystrophic or senescent. While aged microglia have been frequently identified in neurodegenerative diseases such as Alzheimer's disease, there is no conclusive evidence that proves a causal role. This has been hampered by a lack of models of aged microglia. We have recently generated a model of senescent microglia based on the observation that all dystrophic microglia show iron overload. Iron-overloading cultured microglia causes them to take on a senescent phenotype and can cause changes in models of neurodegeneration similar to those observed in patients. This review considers how this model could be used to determine the role of senescent microglia in neurodegenerative diseases.

Original languageEnglish
Pages (from-to)676-688
Number of pages13
JournalJournal of Neurochemistry
Volume151
Issue number6
Early online date3 Sept 2019
DOIs
Publication statusPublished - 1 Dec 2019

Bibliographical note

© 2019 International Society for Neurochemistry.

Funding

Dafina Angelova was supported by PhD Studentship from BRACE. The authors state that there was no conflict of interest in the preparation of this review.

Keywords

  • aging
  • dystrophic
  • iron
  • neurodegeneration
  • SASP

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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