N-Acetylcysteine delays age-associated memory impairment in mice: role in synaptic mitochondria

Mitochondrial oxidative damage is implicated in brain aging and in age-rela ted neurodegenerative diseases. Since N-acetylcysteine (NAC) has recently b een shown to prevent apoptotic death in neuronal cells and protect synaptic mitochondria proteins from oxidative damage in aged mice, we have investig ated whether dietary administration of this thiolic antioxidant retards age -related memory loss. At 48 weeks of age, a control female OF-1 mice group was fed standard food pellets and another group received pellets containing 0.3% (w/w) of NAG. After 23 weeks of this diet, the NAC had partially rest ored the memory deficit associated with aging in mice. Moreover, the Lipid peroxide and protein carbonyl contents of the synaptic mitochondria were si gnificantly decreased in the NAG-supplemented animals in comparison with th eir age-matched controls. The antioxidant properties and probable action on mitochondrial bioenergetic ability in the synaptic terminals may explain, at least partially, the beneficial action of NAC administration. (C) 2000 P ublished by Elsevier Science B.V. All rights reserved.