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Inhibition of stress induced premature senescence in presenilin-1 mutated cells with water soluble Coenzyme Q10.

Inhibition of stress induced premature senescence in presenilin-1 mutated cells with water soluble Coenzyme Q10.

Mitochondrion (2014-07-19)

Dennis Ma, Kyle Stokes, Kevinjeet Mahngar, Danijela Domazet-Damjanov, Marianna Sikorska, Siyaram Pandey

ABSTRACT

A water-soluble formulation of CoQ10 (WS-CoQ10) was shown to stabilize mitochondria and prevent oxidative stress-induced neuronal death. Presenilin-1 (PS-1)-mutated Alzheimer's Disease (AD) fibroblasts (PSAF) were used for studying the effects of PS-1 mutation. PS-1 mutation correlated to increased reactive oxygen species (ROS) production and stress induced premature senescence (SIPS) in PSAF; WS-CoQ10 treatment decreased ROS generation, increased population doublings, and postponed SIPS. Treated PSAF had higher PCNA expression, and lower levels of MnSOD, p21, p16Ink4A, and Rb. WS-CoQ10 caused the resumption of autophagy in PSAF. Thus, WS-CoQ10 as inhibitor of SIPS and ameliorator of autophagy could be an effective prophylactic/therapeutic agent for AD.

MATERIALS

Product Number

Brand

Product Description

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