ArticleFrontiers in molecular neuroscience2019
Injection of α-syn-98 Aggregates Into the Brain Triggers α-Synuclein Pathology and an Inflammatory Response.
Article in Frontiers in molecular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 9 citations in OpenAlex.
- The Role of IL-6 in Neurodegenerative Disorders.Neurochemical research · 2024Review
- SNCA correlates with immune infiltration and serves as a prognostic biomarker in lung adenocarcinoma.BMC cancer · 2022Article
- α-Synuclein at the Presynaptic Axon Terminal as a Double-Edged Sword.Biomolecules · 2022Review
- Article
- SARS-CoV-2 Proteins Interact with Alpha Synuclein and Induce Lewy Body-like Pathology In Vitro.International journal of molecular sciences · 2022Article
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5 authors at 1 institution in 1 country.
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Abstract
Pathological aggregation of α-synuclein (α-syn) is a major component of Lewy bodies (LB), which play a central role in pathogenesis of Parkinson's disease (PD). Differential expression of α-syn isoforms has been shown in PD. Isoform α-syn-98 is generated by excision of exon-3 and exon-5 of the α-syn gene. In contrast to the canonical full-length α-syn isoform (α-syn140), little is known about the function of the α-syn-98 isoform. In the present study, to identify the potential role of α-syn-98 protein in PD, we examined the effects of exogenous recombinant insoluble α-syn-98 aggregates on α-syn pathology and inflammatory responses in the midbrain. After injection of α-syn-98 aggregates into the substantia nigra (SN), mice exhibited motor dysfunction accompanied by nigral dopaminergic neuron loss. In addition, α-syn-98 aggregates injection resulted in a significant increase in phosphorylation of endogenous α-syn. Accumulations of α-syn were co-localized with p62 and ubiquitin, which suggests α-syn-98 aggregates-induced pathology exhibits properties similar to human LB. Many glial cells were activated after α-syn-98 aggregates injection. In addition, expression of NF-κB, interleukin 6 (IL6), and tumor necrosis factor-α (TNF-α) and levels of oxidative stress increased after α-syn-98 aggregates injection. Our results suggest that α-syn-98 may play a crucial role in the pathogenesis of PD.
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