This article examines the functional significance of Ca2+-dependent synapti
c plasticity in relation to compromised memory function during aging, Resea
rch characterizing an age-related decline in memory for tasks that require
proper hippocampal function is summarized, It is concluded that aged animal
s possess the mechanisms necessary for memory formation, and memory deficit
s, including rapid forgetting, result from more subtle changes in memory pr
ocesses for memory storage or maintenance. A review of experimental studies
concerning changes in hippocampal neural plasticity over the course of agi
ng indicates that, during aging, there is a shift in mechanisms that regula
te the thresholds for synaptic modification, including Ca2+ channel functio
n and subsequent Ca2+-dependent processes. The results, combined with theor
etical considerations concerning synaptic modification thresholds, provide
the basis for a model of age-related changes in hippocampal synaptic functi
on. The model is employed as a foundation for interpretation of studies exa
mining therapeutic intervention in age-related memory decline. The possible
role of altered synaptic plasticity thresholds in learning and memory defi
cits suggests that treatments that modify synaptic plasticity may prove fru
itful for the development of early therapeutic interventions in age-related
neurodegenerative diseases. (C) 1999 Elsevier Science B.V, All rights rese
rved.