ABSTRACT
It is becoming increasingly clear that senescence affects intracellular brain signal transduction at a number of different levels, from receptor availability and coupling with effector systems, to production of second messengers and activation of protein kinases. Various observations indicate that Protein Kinase C (PKC) might be a target for the aging process. The increase in PKC in hippocampal structures may represent a compensatory process for reduced synaptic excitability during aging, as indicated by electrophysiological measurements possibly linked to altered intracellular Ca2+ handling. In light of the reported specificity in B-50 phosphorylation by the various PKC isoforms it was important to investigate eventual age-related changes in PKC isoform expression that might explain the substrate-dependent changes in PKC activity during aging. Analysis of PKC activity in the brain of aged good and bad learners could define more easily detected differences in kinase activity correlated with learning capabilities. A variety of observations have demonstrated an involvement of PKC in Alzheimer's disease.
