Makoto Naoi

TL;DR: It is suggested that mitochondrial dysfunction, especially decreased activity of complex I, may reduce proteasome activity through oxidative modification of proteasomes itself and aggregation with other oxidized proteins, which might account for the accumulation of modified protein and, at least partially, for cell death of the dopamine neurons in Parkinson's disease.

TL;DR: Increased oxidative stress caused by SIN-1 treatment induced a decline in the mitochondrial membrane potential, ΔΨm, and activated mitochondrial apoptotic signaling and induced cell death in SH-SY5Y cells, suggesting that neurons are exposed to constant oxidative stress even under physiological conditions.

TL;DR: In this article, Rasagiline induced phosphorylation of inhibitory subunit (IkappaB) and translocation of active p65 subunit from cytoplasm into nuclei.

TL;DR: Novel role of MAOA and serotonin in the pathogenesis and therapy of depressive disorders is discussed, which helps protect neurons from cell death in depression through induction of anti-apoptotic Bcl-2 and prosurvival neurotrophic factors.

TL;DR: The role of polyphenols in regulation of mitochondrial redox state, death signal system, and homeostasis is presented.