Cited by 258Neuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and TreatmentsInflammasome and immune disorders

Aging‐dependent changes of microglial cells and their relevance for neurodegenerative disorders

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Von Bernhardi, Rommy, Tichauer, Juan E., Eugenín, Jaime·2010·Journal of Neurochemistry

Abstract

J. Neurochem. (2010) 112, 1099–1114. Among multiple structural and functional brain changes, aging is accompanied by an increase of inflammatory signaling in the nervous system as well as a dysfunction of the immune system elsewhere. Although the long‐held view that aging involves neurocognitive impairment is now dismissed, aging is a major risk factor for neurodegenerative diseases such as Alzheimer`s disease, Parkinson`s disease and Huntington’s disease, among others. There are many age‐related changes affecting the brain, contributing both to certain declining in function and increased frailty, which could singly and collectively affect neuronal viability and vulnerability. Among those changes, both inflammatory responses in aged brains and the altered regulation of toll like receptors, which appears to be relevant for understanding susceptibility to neurodegenerative processes, are linked to pathogenic mechanisms of several diseases. Here, we review how aging and pro‐inflammatory environment could modulate microglial phenotype and its reactivity and contribute to the genesis of neurodegenerative processes. Data support our idea that age‐related microglial cell changes, by inducing cytotoxicity in contrast to neuroprotection, could contribute to the onset of neurodegenerative changes. This view can have important implications for the development of new therapeutic approaches.

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Crossref · 10.1111/j.1471-4159.2009.06537.x

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  • Immunosenescence and inflammaging can both contribute to neuroinflammation, resulting in impaired neuronal function and the accumulation of brain tissue damage.

    “Immunosenescence and inflammaging can both contribute to neuroinflammation, resulting in impaired neuronal function and the accumulation of brain tissue damage.137,138”

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Authors
Von Bernhardi, R., Tichauer, J. E., & Eugenín, J.
Affiliations
  • Pontificia Universidad Católica de Chile (CL)
  • Universidad de Santiago de Chile (CL)
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2010-02-02
Volume
112
Issue
5
Pages
1099-1114
ISSN
  • 0022-3042 (ISSN-L)
  • 1471-4159
OpenAlex
W2027368264
Cited by
258
References
203
Citations by year
2026: 2 · 2025: 11 · 2024: 16 · 2023: 14 · 2022: 13 · 2021: 21 · 2020: 20 · 2019: 19 · 2018: 18 · 2017: 13 · 2016: 15 · 2015: 16 · 2014: 10 · 2013: 22 · 2012: 23
FWCI
1.24
Type
journal article
Language
en
Open access
Locations
  • Journal of Neurochemistry (publishedVersion)
  • PubMed (publishedVersion)
  • Americanae (AECID Library) (submittedVersion, other-oa)
  • LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Keywords
microglia, brain aging, neuroinflammation, neurodegenerative diseases, Toll-like receptors, microglial phenotype, Alzheimer's disease, Parkinson's disease, Huntington's disease, neuroprotection, cytotoxicity, neurodegeneration
MeSH terms
Aging, Animals, Brain, Disease Models, Animal, Humans, Iron, Gene Expression, Cytokines, Microglia, Oxidative Stress, Neurodegenerative Diseases

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