Oishimaya Sen

TL;DR: It is suggested that intracellularly accumulated α‐synuclein can interact with mitochondria in intact SHSY5Y cells causing dysfunction of the organelle which drives the cell death under the authors' experimental conditions, which has clear implications in the pathogenesis of sporadic Parkinson's disease.

TL;DR: DA cytotoxicity includes both oxidative and nonoxidative modes and may involve overexpression and accumulation of alpha-synuclein as well as proteasomal inhibition.

TL;DR: Higher serum ADA, triglycerides (TG) and fasting plasma glucose (FPG) levels in nonobese T2DM patients, and a strong correlation betweenADA and FPG which suggests an association between ADA and nonobesity T2 DM subjects are shown.

TL;DR: It is demonstrated that iron causes an increase in α-synuclein content in SH-SY5Y cells associated with mitochondrial depolarization, decreased cellular ATP content and loss of cell viability during incubation up to 96 h, and knocking-down α- synuclein expression prevents cytotoxic actions of iron.

TL;DR: Dopamine-induced mitochondrial dysfunction and the loss of cell viability under experimental conditions could be prevented by cyclosporine, a blocker of mitochondrial permeability transition pore, as well as the antioxidant N-acetylcysteine, and the dopamine effects on cell viability and mitochondrial functions were significantly prevented by knocking down α-synuclein expression by specific siRNA.