ArticleGlia2020
Microglia senescence occurs in both substantia nigra and ventral tegmental area.
Article in Glia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- LaminA/C-dependent cellular senescence signaling promotes skeletal muscle atrophy and abnormalities in Parkinson's disease.Cell death & disease · 2026Article
- Beyond biochemical cascades: novel bio-mechanical and epigenetic paradigms of glial SASP in brain aging.Metabolic brain disease · 2026Review
- From Neuron-Centric to Glia-Centric: How Aging Glial Networks Drive Neurodegenerative Disease.Journal of neurochemistry · 2026Review
- Cranial radiotherapy profoundly affects glia without inducing widespread cellular senescence.Neuro-oncology · 2025Article
- Alzheimer's Disease: From Molecular Mechanisms to Promising Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Autophagy and Cellular Senescence in Alzheimer's Disease: Key Drivers of Neurodegeneration.CNS neuroscience & therapeutics · 2025Review
- FKBP51 inhibition ameliorates neurodegeneration and motor dysfunction in the neuromelanin-SNCA mouse model of Parkinson's disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Cellular senescence in Alzheimer's disease: from physiology to pathology.Translational neurodegeneration · 2024Review
- Microglial senescence in neurodegeneration: Insights, implications, and therapeutic opportunities.Neuroprotection (Chichester, England) · 2024Article
- Role of microglia in diabetic neuropathic pain.Frontiers in cell and developmental biology · 2024Review
- Transcriptional and epigenetic decoding of the microglial aging process.Nature aging · 2023Article
- Interleukin-10 enhances activity of ventral tegmental area dopamine neurons resulting in increased dopamine release.Brain, behavior, and immunity · 2023Article
- Age-Related Modifications of Electroencephalogram Coherence in Mice Models of Alzheimer's Disease and Amyotrophic Lateral Sclerosis.Biomedicines · 2023Article
- The complex role of inflammation and gliotransmitters in Parkinson's disease.Neurobiology of disease · 2023Review
- Role of Microglia in Psychostimulant Addiction.Current neuropharmacology · 2023Review
- Cellular senescence: the good, the bad and the unknown.Nature reviews. Nephrology · 2022Review
- Photoinduced elimination of senescent microglia cellsChemical science · 2022Article
- Microglia Drive Pockets of Neuroinflammation in Middle Age.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Glial TDP-43 and TDP-43 induced glial pathology, focus on neurodegenerative proteinopathy syndromes.Glia · 2022Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
During aging humans lose midbrain dopamine neurons, but not all dopamine regions exhibit vulnerability to neurodegeneration. Microglia maintain tissue homeostasis and neuronal support, but microglia become senescent and likely lose some of their functional abilities. Since aging is the greatest risk factor for Parkinson's disease, we hypothesized that aging-related changes in microglia and neurons occur in the vulnerable substantia nigra pars compacta (SNc) but not the ventral tegmental area (VTA). We conducted stereological analyses to enumerate microglia and dopaminergic neurons in the SNc and VTA of 1-, 6-, 9-, 18-, and 24-month-old C57BL/J6 mice using sections double-stained with tyrosine hydroxylase (TH) and Iba1. Both brain regions show an increase in microglia with aging, whereas numbers of TH+ cells show no significant change after 9 months of age in SNc and 6 months in VTA. Morphometric analyses reveal reduced microglial complexity and projection area while cell body size increases with aging. Contact sites between microglia and dopaminergic neurons in both regions increase with aging, suggesting increased microglial support/surveillance of dopamine neurons. To assess neurotrophin expression in dopaminergic neurons, BDNF and TH mRNA were quantified. Results show that the ratio of BDNF to TH decreases in the SNc, but not the VTA. Gait analysis indicates subtle, aging-dependent changes in gait indices. In conclusion, increases in microglial cell number, ratio of microglia to dopamine neurons, and contact sites suggest that innate biological mechanisms compensate for the aging-dependent decline in microglia morphological complexity (senescence) to ensure continued neuronal support in the SNc and VTA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.