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- W2801299411 abstract "Increasing evidence suggests a relationship between oxidative stress and α-synuclein aggregation, the primary pathological hallmark of Parkinson disease (PD). However, a direct causal relationship has not yet been established in vivo in mouse models of PD. Superoxide dismutase 2 (SOD2) is rate limiting in the antioxidant machinery of the mitochondria and even its partial deficiency elevates oxidative stress in mice. Therefore, in order to investigate a possible interaction between oxidative stress and α-synuclein aggregation in vivo, a transgenic model of PD with haplodeficiency for SOD2 was generated on the basis of the well-characterized murine (Thy-1)-h[A30P]-α-synuclein transgenic line. In comparison with littermate controls with full SOD2 capacity, α-synuclein transgenic mice with partial SOD2 deficiency exhibited a significantly more advanced stage of synucleinopathy at 16 months, as demonstrated by higher median PK-PET blot scores (p < 0.01) and a greater amount of truncated α-synuclein in the insoluble fraction of homogenized brains (p < 0.05). These results show that compromising the capacity to scavenge free radicals can exacerbate α-synuclein aggregation, indicating that elevated levels of oxidative stress could modulate the progression of PD." @default.
- W2801299411 created "2018-05-17" @default.
- W2801299411 creator A5036705607 @default.
- W2801299411 creator A5042918992 @default.
- W2801299411 date "2018-04-27" @default.
- W2801299411 modified "2023-10-17" @default.
- W2801299411 title "Increased Oxidative Stress Exacerbates α-Synuclein Aggregation In Vivo" @default.
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- W2801299411 doi "https://doi.org/10.1093/jnen/nly024" @default.
- W2801299411 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29718367" @default.
- W2801299411 hasPublicationYear "2018" @default.
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