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Microglial dysfunction in brain aging and Alzheimer's disease

Kira Irving Mosher1, Tony Wyss-Coray2

  • 1Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA; Neuroscience IDP Program, Stanford University School of Medicine, Stanford, California 94305, USA.

Biochemical Pharmacology
|January 22, 2014
PubMed

Insights

Microglia, the brain's immune cells, show similar changes in Alzheimer's disease (AD) and aging. This review details six microglial functions affected by both conditions to guide future research.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Microglia are central nervous system immune cells implicated in Alzheimer's disease (AD) pathophysiology.
  • Recent genetic studies highlight the significance of microglial molecules in AD.
  • Microglia in aging and AD brains share phenotypes, but their combined impact is understudied.

Purpose of the Study:

  • To review the distinct functions of microglia.
  • To discuss the specific effects of aging and Alzheimer's disease on these functions.
  • To identify commonalities between aging and AD states in microglia to inspire new research.

Main Methods:

  • Literature review and synthesis of existing research on microglia.
  • Enumeration of six distinct microglial functions.
  • Comparative analysis of microglial phenotypes in aging and AD.

Main Results:

  • Microglia exhibit altered functions in both aging and AD.
  • Commonalities exist in microglial responses to aging and AD.
  • The concepts of microglial "activation" and "neuroinflammation" are complex and encompass multiple processes.

Conclusions:

  • Understanding shared microglial mechanisms in aging and AD is crucial.
  • This review provides a framework for dissecting microglial functions in neurodegeneration.
  • New research approaches can be inspired by considering aging and AD impacts on microglia together.
Keywords:
AgingAlzheimer's diseaseMicrogliaNeurodegenerationNeuroinflammation

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