Effects of age and caloric restriction on brain neuronal cell death/survival

Annals of the New York Academy of Sciences
Asimina Hiona, Christiaan Leeuwenburgh

Abstract

Aging may pose a challenge to the central nervous system, increasing its susceptibility to apoptotic events. Recent findings indicate that caloric restriction (CR) may have a profound effect on brain function and vulnerability to injury and diseases, by enhancing neuroprotection, stimulating the production of new neurons, and increasing synaptic plasticity. Apoptosis and apoptotic regulatory proteins in the brain frontal cortex of 6-month-old ad libitum fed (6AD), 26-month-old ad libitum fed (26AD), and 26-month-old caloric-restricted (26CR) male Fischer 344 rats (40% restriction compared to ad libitum fed) were investigated. Levels of Poly-ADP ribose polymerase (PARP-DNA repair enzyme; its cleaved 89 kDA fragment is a marker of apoptosis), cytoplasmic histone-associated DNA fragments, and X chromosome-linked inhibitor of apoptosis (XIAP--an endogenous apoptosis inhibitor) were determined. A significant age-associated increase in PARP was found, which was ameliorated in the frontal cortices of the CR rats. No significant differences in cytoplasmic histone-associated DNA fragments with age or with CR were observed. XIAP levels significantly increased with age in the brains of the ad libitum animals, while CR animals exhibited th...Continue Reading

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis