Age-related changes in heat shock protein expression in the mouse hippocampus

Abstract

Heat shock proteins (Hsps) serve as the cell's natural mechanism for circumventing protein misfolding and aggregation often involved in cellular stress. These stressors can lead to neurodegenerative pathologies like Alzheimer's disease (AD). Research suggests that aged animals lose the ability to upregulate Hsps in response to an acute stress, and this disregulation may contribute to the onset of AD. We hypothesize that aged animals will show elevated Hsp levels due to the increase in cellular stress associated with aging. We further hypothesize that this increased level of Hsps will inhibit the aged animal from further expressing Hsps in the event of an acute stress. We compared basal and inducible brain hippocampus levels of four Hsps previously shown to stabilize two proteins commonly associated with AD, amyloid beta and tau. Our results support our hypothesis that Hsp expression changes with age and may be a contributing factor in AD.