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

Mitochondrion. 2014 Jul:17:106-15. doi: 10.1016/j.mito.2014.07.004. Epub 2014 Jul 15.

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.

Keywords: Alzheimer's disease; Autophagy; Coenzyme Q(10); Mitochondria; Reactive oxygen species; Senescence.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging*
  • Alzheimer Disease
  • Cells, Cultured
  • Female
  • Fibroblasts / drug effects*
  • Fibroblasts / physiology*
  • Humans
  • Male
  • Presenilin-1 / deficiency*
  • Stress, Physiological*
  • Ubiquinone / analogs & derivatives*
  • Ubiquinone / metabolism
  • Vitamins / metabolism*

Substances

  • Presenilin-1
  • Vitamins
  • Ubiquinone
  • coenzyme Q10