If you’ve ever struggled to remember a phone number 30 seconds after learning it or calculate — in your head — the 15 percent tip at dinner, you’re not alone. Most of us will struggle with these tasks at some point, and it has nothing to do with our ability with numbers. Age-related memory loss is an inevitable but variable phenomenon. Generally speaking, however, the graph on age-related memory loss through the decades of life is not very interesting, says University of Florida neuroscience professor Jennifer Bizon — until we hit our 70s: Then the slow, steady decline that began in our 20s speeds up to a more precipitous decline. see full article at
Published March 5th, 2014 in UF News, University of Florida
“UF researchers find drug therapy that could eventually reverse memory decline in seniors”
GAINESVILLE, Fla. — It may seem normal: As we age, we misplace car keys, or can’t remember a name we just learned or a meal we just ordered. But University of Florida researchers say memory trouble doesn’t have to be inevitable, and they’ve found a drug therapy that could potentially reverse this type of memory decline.
The drug can’t yet be used in humans, but the researchers are pursuing compounds that could someday help the population of aging adults who don’t have Alzheimer’s or other dementias but still have trouble remembering day-to-day items. Their findings will be published in today’s (March 5) issue of the Journal of Neuroscience. see full UF News article at:
“Prefrontal Cortical GABAergic Dysfunction Contributes to Age-Related Working Memory Impairment “
Cristina Bañuelos, B. Sofia Beas, Joseph A. McQuail, Ryan J. Gilbert, Charles J. Frazier, Barry Setlow, and Jennifer L. Bizon.
Working memory functions supported by the prefrontal cortex decline in normal aging. Disruption of corticolimbic GABAergic inhibitory circuits can impair working memory in young subjects; however, relatively little is known regarding how aging impacts prefrontal cortical GABAergic signaling and whether such changes contribute to cognitive deficits. The current study used a rat model to evaluate the effects of aging on expression of prefrontal GABAergic synaptic proteins in relation to working memory decline, and to test whether pharmacological manipulations of prefrontal GABAergic signaling can improve working memory abilities in aged subjects. Results indicate that in aged medial prefrontal cortex (mPFC), expression of the vesicular GABA transporter VGAT was unchanged; however, there was a significant increase in expression of the GABA synthesizing enzyme GAD67, and a significant decrease in the primary neuronal GABA transporter GAT-1 and in both subunits of the GABA(B) receptor (GABA(B)R). Expression of VGAT, GAD67, and GAT-1 was not associated with working memory ability. In contrast, among aged rats, GABA(B)R expression was significantly and negatively associated with working memory performance, such that lower GABA(B)R expression predicted better working memory. Subsequent experiments showed that systemic administration of a GABA(B)R antagonist, CGP55845, dose-dependently enhanced working memory in aged rats. This enhancing effect of systemic CGP55845 was reproduced by direct intra-mPFC administration. Together, these data suggest that age-related dysregulation of GABAergic signaling in prefrontal cortex may play a causal role in impaired working memory and that targeting GABA(B)Rs may provide therapeutic benefit for age-related impairments in executive functions.