Parkinson’s disease as a result of aging
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Summary: It is generally considered that Parkinson's disease is induced by specific agents that degenerate a clearly defined population of dopaminergic neurons. Data commented in this review suggest that this assumption is not as clear as is often thought and that aging may be critical for Parkinson's disease. Neurons degenerating in Parkinson's disease also degenerate in normal aging, and the different agents involved in the etiology of this illness are also involved in aging. Senescence is a wider phenomenon affecting cells all over the body, whereas Parkinson's disease seems to be restricted to certain brain centers and cell populations. However, reviewed data suggest that Parkinson's disease may be a local expression of aging on cell populations which, by their characteristics (high number of synaptic terminals and mitochondria, unmyelinated axons, etc.), are highly vulnerable to the agents promoting aging. The development of new knowledge about Parkinson's disease could be accelerated if the research on aging and Parkinson's disease were planned together, and the perspective provided by gerontology gains relevance in this field.
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α-Synuclein-induced abnormal upregulation of TH phosphorylation, combined with reduction of gene transcription by aging and aging-related disorders, accelerates pSer40-TH degradation to reduce total TH protein.
“The α-synuclein-induced abnormal upregulation of TH phosphorylation, combined with the reduction of gene transcription by aging and aging-related disorders [126,127,128,129], results in the acceleration of pSer40-TH degradation to reduce total TH protein (Figure 3).”
From Degradation of Tyrosine Hydroxylase by the Ubiquitin-Proteasome System in the Pathogenesis of Parkinson’s Disease and Dopa-Responsive Dystonia (2020) · cites this paper as [129]
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Research works printed but not linked: 1
- Lauri A Pompilio G Capogrossi MC The mitochondrial genome in aging and senescence Ageing Res. Rev 2014b 18C 1 15 25042573
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Hypoxia signaling in human health and diseases: implications and prospects for therapeutics
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Diaminodiphenyl sulfone–induced parkin ameliorates age-dependent dopaminergic neuronal loss
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- Authors
- Rodriguez, M., Rodriguez‐Sabate, C., Morales, I., Sanchez, A., & Sabate, M.
- Affiliations
- Laboratory of Neurobiology and Experimental Neurology Department of Physiology Faculty of Medicine University of La Laguna La Laguna Spain
- Biomedical Research Networking Center on Neurodegenerative Diseases (ES)
- Rehabilitation Service Department of Pharmacology and Physical Medicine Faculty of Medicine University of La Laguna La Laguna Spain
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2015-02-09
- Volume
- 14
- Issue
- 3
- Pages
- 293-308
- ISSN
- 1474-9718 (ISSN-L)
- 1474-9726
- PMC
- PMC4406659
- OpenAlex
- W2037891639
- Cited by
- 214
- References
- 396
- Citations by year
- 2026: 2 · 2025: 21 · 2024: 22 · 2023: 17 · 2022: 13 · 2021: 23 · 2020: 25 · 2019: 16 · 2018: 28 · 2017: 16 · 2016: 20 · 2015: 11
- FWCI
- 3.29
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Aging Cell (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Centro de Investigacion Biomedica en Red Enfermedades Neurodegenerativas, CIBERNED (2014/06)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- Parkinson's disease, aging, dopaminergic neurons, neurodegeneration, cellular senescence, mitochondrial vulnerability, synaptic terminals, unmyelinated axons, gerontology, etiology of Parkinson's disease
- MeSH terms
- Aging, Animals, Brain, Dopamine, Humans, Mitochondria, Neurons, Parkinson Disease
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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