Abstract
The senescence-accelerated prone (SAMP8) mouse model shows age-dependent deterioration in learning and memory and increased oxidative stress in the brain. We previously showed that healthy subjects on a six-week supplementation of a chicken meat hydrolysate (ProBeptigen®/CMI-168) demonstrated enhanced and sustained cognitive performance up until two weeks after the termination of supplementation. In this study, we investigate the effect of ProBeptigen on the progression of age-related cognitive decline. Three-month old SAMP8 mice were orally administered different doses of ProBeptigen (150,300 or 600 mg/kg/day) or saline daily for 13 weeks. Following ProBeptigen supplementation, mice showed lower scores of senescence and improved learning and memory in avoidance tasks. ProBeptigen treatment also increased antioxidant enzyme activity and dopamine level while reducing protein and lipid peroxidation and mitochondrial DNA damage in the brain. Microarray analysis of hippocampus revealed several processes that may be involved in the improvement of cognitive ability by ProBeptigen, including heme binding, insulin growth factor (IGF) regulation, carboxylic metabolic process, oxidation–reduction process and endopeptidase inhibition. Genes found to be significantly altered in both ProBeptigen treated male and female mice include Mup1, Mup17, Mup21, Ahsg and Alb. Taken together, these results suggest a potential anti-aging effect of ProBeptigen in alleviating cognitive deficits and promoting the antioxidant defense system.
Highlights
Aging is an inevitable process that may be accompanied by neurodegeneration [1,2,3] leading to cognitive decline [4,5,6]
There are a few hallmarks of brain aging, including a decreased antioxidant defense, increased oxidative stress and an impaired mitochondrial oxidative phosphorylation (OXPHOS) system leading to mitochondrial dysfunction [9]
A wide variety of compounds with anti-oxidative properties have been reported to be able to prolong life span, improve learning and memory disorders and reverse the measures of oxidative stress in SAMP8 mice [14,18,19,33,34,35,36,37]. All these findings suggest that oxidative stress plays a role in the memory dysfunction of SAMP8 mice
Summary
Aging is an inevitable process that may be accompanied by neurodegeneration [1,2,3] leading to cognitive decline [4,5,6]. Mitochondrial dysfunction plays a major role in both the physiological aging process and neurodegeneration [12,13] by generating reactive oxygen species (ROS). This concept has been termed the free radical theory of aging. ROS can lead to oxidative stress induction and damage accumulation such as through DNA mutation or lipid and protein dysfunction [9,14], all of which may contribute to age-related neurodegenerative disorders [15]
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