The DOI matches its Crossref record; 233 of the 233 references it cites were found in a registry or an index.
Role of α-Synuclein in Inducing Innate and Adaptive Immunity in Parkinson Disease
Open accessAbstract
Alpha-synuclein (α-syn) is central to the pathogenesis of Parkinson disease (PD). Gene duplications, triplications and point mutations in SNCA1, the gene encoding α-syn, cause autosomal dominant forms of PD. Aggregated and post-translationally modified forms of α-syn are present in Lewy bodies and Lewy neurites in both sporadic and familial PD, and recent work has emphasized the prion-like ability of aggregated α-syn to produce spreading pathology. Accumulation of abnormal forms of α-syn is a trigger for PD, but recent evidence suggests that much of the downstream neurodegeneration may result from inflammatory responses. Components of both the innate and adaptive immune systems are activated in PD, and influencing interactions between innate and adaptive immune components has been shown to modify the pathological process in animal models of PD. Understanding the relationship between α-syn and subsequent inflammation may reveal novel targets for neuroprotective interventions. In this review, we examine the role of α-syn and modified forms of this protein in the initiation of innate and adaptive immune responses.
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“There is evidence for α-synuclein misfolding and aggregation being promoted by an inflammatory microenvironment that subsequently induces an immune response and further inflammation to create a vicious and disease-promoting positive feedback loop [118–120].”
From The gut–brain axis in early Parkinson’s disease: from prodrome to prevention (2025) · cites this paper as [118]
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“Production of neuroinflammation may trigger α-syn oligomerization, leading to a harmful cycle of microglial activation.”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [237]
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“Remarkably, neuroinflammation induced by α-syn may occur even before the loss of dopaminergic neurons in PD.”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [237]
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Metadata
- Authors
- Allen Reish, H. E., & Standaert, D. G.
- Affiliations
- Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Alabama, USA
- University of Alabama at Birmingham (US)
- ORCID
- Standaert, David G.
- Venue
- Journal of Parkinson’s Disease
- Publisher
- SAGE Publications
- Published
- 2015-01-01
- Volume
- 5
- Issue
- 1
- Pages
- 1-19
- ISSN
- 1877-7171 (ISSN-L)
- 1877-718X
- PMC
- PMC4405142
- OpenAlex
- W1480927111
- Cited by
- 244
- References
- 233
- Citations by year
- 2026: 11 · 2025: 20 · 2024: 30 · 2023: 20 · 2022: 26 · 2021: 39 · 2020: 20 · 2019: 19 · 2018: 18 · 2017: 18 · 2016: 16 · 2015: 7
- FWCI
- 13.71
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Parkinson s Disease (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute of Neurological Disorders and Stroke (F31NS076017)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Keywords
- alpha-synuclein, Parkinson's disease, innate immunity, adaptive immunity, neuroinflammation, Lewy bodies, Lewy neurites, prion-like spreading, post-translational modification, neurodegeneration, neuroprotection
- MeSH terms
- Humans, Immunity, Innate, Parkinson Disease, alpha-Synuclein, Adaptive Immunity
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