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Alpha-synuclein: Pathology, mitochondrial dysfunction and neuroinflammation in Parkinson’s disease

Open access
Rocha, Emily M., De Miranda, Briana, Sanders, Laurie H.·2018·Neurobiology of Disease

Abstract

Parkinson's disease (PD) is a complex, chronic and progressive neurodegenerative disease. While the etiology of PD is likely multifactorial, the protein α-synuclein is a central component to the pathogenesis of the disease. However, the mechanism by which α-synuclein causes toxicity and contributes to neuronal death remains unclear. Mitochondrial dysfunction is also widely considered to play a major role in the underlying mechanisms contributing to neurodegeneration in PD. This review discusses evidence for the neuropathological role for α-synuclein in the dysfunction of dopamine neurons in PD. We also discuss insights into the structure, localization, and cellular roles for α-synuclein that may influence its aggregation properties, ultimately impacting its pathogenicity, role in lysosomal dysfunction and activation of the neuroimmune response. We further highlight recent evidence linking α-synuclein and mitochondrial dysfunction in neurodegeneration. Identifying the underlying mechanisms responsible for this bi-directional relationship between α-synuclein and mitochondrial dysfunction may provide new insights into the pathophysiology of PD.

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Metadata

Authors
Rocha, E. M., De Miranda, B., & Sanders, L. H.
Venue
Neurobiology of Disease
Publisher
Elsevier BV
Published
2018-01
Volume
109
Issue
Pt B
Pages
249-257
ISSN
0969-9961 (ISSN-L)
OpenAlex
W2605252223
Cited by
762
References
24
FWCI
28.15
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Alpha-synuclein: Pathology, mitochondrial dysfunction and neuroinflammation in Parkinson’s disease. https://app.cochat.ai/papers/10.1016/j.nbd.2017.04.004
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Rocha, E. M., De Miranda, B., & Sanders, L. H. (2018). Alpha-synuclein: Pathology, mitochondrial dysfunction and neuroinflammation in Parkinson’s disease. Neurobiology of Disease. https://doi.org/10.1016/j.nbd.2017.04.004

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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