The DOI matches its Crossref record; 85 of the 85 references it cites were found in a registry or an index.
Microglia in the aging brain: relevance to neurodegeneration
Open accessAbstract
Microglia cells are the brain counterpart of macrophages and function as the first defense in the brain. Although they are neuroprotective in the young brain, microglia cells may be primed to react abnormally to stimuli in the aged brain and to become neurotoxic and destructive during neurodegeneration. Aging-induced immune senescence occurs in the brain as age-associated microglia senescence, which renders microglia to function abnormally and may eventually promote neurodegeneration. Microglia senescence is manifested by both morphological changes and alterations in immunophenotypic expression and inflammatory profile. These changes are likely caused by microinvironmental factors, but intrinsic factors cannot yet be completely excluded. Microglia senescence appears to underlie the switching of microglia from neuroprotective in the young brain to neurotoxic in the aged brain. The hypothesis of microglia senescence during aging offers a novel perspective on their roles in aging-related neurodegeneration. In Parkinson's disease and Alzheimer's disease, over-activation of microglia may play an active role in the pathogenesis because microglia senescence primes them to be neurotoxic during the development of the diseases.
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“The ageing brain is also characterised by structural and functional changes to microglial cells, which are the resident immune cell population of the central nervous system (CNS) and are the CNS equivalent of macrophages. They are activated by brain injury and local and systemic inflammation and become primed (hyper-responsive) to small stimuli with ageing, which can potentially cause damage and”
From Frailty in elderly people (2013) · cites this paper as [26]
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Metadata
- Authors
- Luo, X.-G., Ding, J.-Q., & Chen, S.-D.
- Venue
- Molecular Neurodegeneration
- Published
- 2010-03-24
- Volume
- 5
- Issue
- 1
- Pages
- 12-12
- ISSN
- 1750-1326 (ISSN-L)
- PMC
- PMC2852379
- OpenAlex
- W2156427445
- Cited by
- 236
- References
- 85
- Citations by year
- 2026: 7 · 2025: 12 · 2024: 10 · 2023: 11 · 2022: 17 · 2021: 14 · 2020: 15 · 2019: 11 · 2018: 20 · 2017: 13 · 2016: 18 · 2015: 19 · 2014: 12 · 2013: 22 · 2012: 15
- FWCI
- 10.86
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Molecular Neurodegeneration (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- microglia, brain aging, neurodegeneration, microglial senescence, immunosenescence, neuroinflammation, neuroprotection, Parkinson's disease, Alzheimer's disease, microglial activation, neurotoxicity
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