Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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.

Type

Journal article

Journal

Brain Res Mol Brain Res

Publication Date

31/05/2000

Volume

78

Pages

154 - 162

Keywords

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