Parkinson’s disease: genetics and pathogenesis
Abstract
Recent investigation into the mechanisms of Parkinson's disease (PD) has generated remarkable insight while simultaneously challenging traditional conceptual frameworks. Although the disease remains defined clinically by its cardinal motor manifestations and pathologically by midbrain dopaminergic cell loss in association with Lewy bodies, it is now recognized that PD has substantially more widespread impact, causing a host of nonmotor symptoms and associated pathology in multiple regions throughout the nervous system. Further, the discovery and validation of PD-susceptibility genes contradict the historical view that environmental factors predominate, and blur distinctions between familial and sporadic disease. Genetic advances have also promoted the development of improved animal models, highlighted responsible molecular pathways, and revealed mechanistic overlap with other neurodegenerative disorders. In this review, we synthesize emerging lessons on PD pathogenesis from clinical, pathological, and genetic studies toward a unified concept of the disorder that may accelerate the design and testing of the next generation of PD therapies.
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Recessively inherited loss-of-function mutations in PINK1 and PRKN are the most common genetic causes of early-onset PD, which occurs in about 5%-10% of cases.
“Recessively inherited loss-of-function mutations in PTEN-induced kinase 1 (PINK1) and the E3 ubiquitin ligase PRKN are the most common genetic causes for early-onset PD, which occurs in about 5%–10% of cases [1, 2].”
From miRNA family miR-29 inhibits PINK1-PRKN signaling via ATG9A (2026) · cites this paper as [1]
Loss-of-function mutations in PINK1 and PRKN result in early-onset Parkinson disease.
“Loss-of-function mutations in the genes encoding PINK1 and PRKN result in early-onset Parkinson disease (EOPD).”
From miRNA family miR-29 inhibits PINK1-PRKN signaling via ATG9A (2026) · cites this paper as [1]
A complex interplay of genetic and environmental factors is thought to drive the pathogenesis of PD, eventually leading to mitochondrial and autophagic dysfunction.
“A complex interplay of genetic and environmental factors is thought to drive the pathogenesis of PD, eventually leading to mitochondrial and autophagic dysfunction (Shulman et al., 2011).”
From Microbiome–microglia connections via the gut–brain axis (2019) · cites this paper as Shulman et al., 2011
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- Authors
- Shulman, J. M., De Jager, P. L., & Feany, M. B.
- Affiliations
- Broad Institute (US)
- Departments of Neurology, Boston, Massachusetts 02115;
- Departments of Pathology, Brigham and Women's Hospital, Boston, Massachusetts 02115;
- ORCID
- Shulman, Joshua M.
- Venue
- Annual Review of Pathology: Mechanisms of Disease
- Publisher
- Annual Reviews
- Published
- 2011-02-28
- Volume
- 6
- Issue
- 1
- Pages
- 193-222
- ISSN
- 1553-4006 (ISSN-L)
- 1553-4014
- OpenAlex
- W2129917779
- Cited by
- 801
- References
- 176
- Citations by year
- 2026: 10 · 2025: 21 · 2024: 42 · 2023: 34 · 2022: 64 · 2021: 64 · 2020: 46 · 2019: 59 · 2018: 54 · 2017: 59 · 2016: 74 · 2015: 64 · 2014: 56 · 2013: 65 · 2012: 52
- FWCI
- 8.22
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annual Review of Pathology Mechanisms of Disease (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Health Sciences › Medicine › Neurology › Neurological disorders and treatments
- Keywords
- Parkinson's disease, susceptibility genes, pathogenesis, dopaminergic neuron loss, Lewy bodies, non-motor symptoms, animal models, neurodegeneration, molecular pathways
- MeSH terms
- Animals, Humans, Parkinson Disease, Lewy Bodies, Genetic Predisposition to Disease
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