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A major focus of aging research has been the search for treatments that will prevent or ameliorate the memory deficits associated with aging. One paradigm, lifelong caloric restriction, has been reported to reduce some of the effects of aging. In the current report, we examined the effects of this treatment on age-related deficits in LTP, a putative cellular building block for memory formation. We report here that lifelong caloric restriction completely prevents the age-related deficit in LTP. In addition, we report that there is a dramatic decrease in the expression of the NMDA receptor subunit NR1 in aged rats and this age-related defect is also prevented by caloric restriction. These data provide a molecular and cellular mechanism by which life long caloric restriction may ameliorate some of the cognitive deficits associated with the aging process.


Journal article


Brain Res Mol Brain Res

Publication Date





154 - 162


Aging, Animals, Cognition Disorders, DNA Primers, Energy Intake, Excitatory Postsynaptic Potentials, Gene Expression, Hippocampus, Long-Term Potentiation, Memory, Memory Disorders, Rats, Rats, Inbred F344, Receptors, N-Methyl-D-Aspartate, Reverse Transcriptase Polymerase Chain Reaction