Aggregation of alph-synuclein in Lewy bodies of sporadic Parkinsons disease and dementia with Lewy bodies

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Aggregation of alph-synuclein in Lewy bodies of sporadic Parkinsons disease and dementia with Lewy bodies. (±)-Ibipinabant at protecting cells against the cytotoxicity of -synuclein. These strategies may lead to the development of therapeutic agents that could prove useful in combating this disease. as well as to demonstrate neurotoxicity in rat PC12 cells [31]. As with other amyloid fibril forming polypeptides, the kinetics of amyloidogenesis implies a nucleation-dependent polymerization with three phases: a lag phase, a growth phase, and a final plateau in fibril formation as measured by thiolflavin T (ThT) fluorescence experiments [32]. Insights from Mutational Studies of -syn One characteristic of early onset PD has been the duplication or triplication of the gene locus for -synuclein resulting in overproduction of the protein [33, 34]. This likely reflects the concentration…
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