Aging causes morphological alterations in astrocytes and microglia in human substantia nigra pars compacta
Abstract
Age being a risk factor for Parkinson's disease, assessment of age-related changes in the human substantia nigra may elucidate its pathogenesis. Increase in Marinesco bodies, α-synuclein, free radicals and so forth in the aging nigral neurons are clear indicators of neurodegeneration. Here, we report the glial responses in aging human nigra. The glial numbers were determined on Nissl-stained sections. The expression of glial fibrillary acidic protein, S100β, 2', 3'-cyclic nucleotide 3' phosphodiesterase, and Iba1 was assessed on cryosections of autopsied midbrains by immunohistochemistry and densitometry. The glial counts showed a biphasic increase, of which, the first prominent phase from fetal age to birth could be physiological gliogenesis whereas the second one after middle age may reflect mild age-related gliosis. Astrocytic morphology was altered, but glial fibrillary acidic protein expression increased only mildly. Presence of type-4 microglia suggests possibility of neuroinflammation. Mild reduction in 2', 3'-cyclic nucleotide 3' phosphodiesterase-labeled area denotes subtle demyelination. Stable age-related S100β expression indicates absence of calcium overload. Against the expected prominent gliosis, subtle age-related morphological alterations in human nigral glia attribute them a participatory role in aging.
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Aged human brains display only mild and heterogeneous changes in astrocyte morphology or GFAP levels.
“Aged human brains display only mild and heterogeneous changes in astrocyte morphology or GFAP levels86.”
From Reactive astrocyte nomenclature, definitions, and future directions (2021) · cites this paper as [86]
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- Authors
- Jyothi, H. J., Vidyadhara, D. J., Mahadevan, A., Philip, M., Parmar, S. K., Manohari, S. G., Shankar, S. K., Raju, T. R., & Alladi, P. A.
- Affiliations
- National Institute of Mental Health and Neurosciences (IN)
- Corresponding author
- Alladi, Phalguni Anand
- ORCID
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2015-12
- Volume
- 36
- Issue
- 12
- Pages
- 3321-3333
- ISSN
- 0197-4580 (ISSN-L)
- OpenAlex
- W1217233333
- Cited by
- 139
- References
- 63
- Citations by year
- 2026: 7 · 2025: 18 · 2024: 5 · 2023: 21 · 2022: 12 · 2021: 17 · 2020: 15 · 2019: 18 · 2018: 12 · 2017: 7 · 2016: 7
- FWCI
- 4.80
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Council for Scientific and Industrial Research (27(0884)/09)
- ICMR (5/4-5/8/Neuro/2009-NCD-I)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- substantia nigra pars compacta, aging, astrocytes, microglia, glial morphology, glial fibrillary acidic protein, S100β, CNPase, Iba1, gliosis, demyelination, neuroinflammation, Parkinson's disease risk
- MeSH terms
- Adolescent, Adult, Aged, Aged, 80 and over, Aging, Astrocytes, Calcium, Child, Child, Preschool, Female, Glial Fibrillary Acidic Protein, Humans, Infant, Male, Middle Aged, Nerve Degeneration, Parkinson Disease, Risk Factors, Microglia, Neurogenic Inflammation, Young Adult, 2',3'-Cyclic Nucleotide 3'-Phosphodiesterase, S100 Calcium Binding Protein beta Subunit, Pars Compacta
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