It's a protein called RbAp48. And, without it, memory loss is a lot more likely to happen as you age. Or so says a new Columbia University report that identified this protein in the brain as the key to reversing the memory loss that can come with old age.
Deficiency of RbAp48 in the hippocampus appears to significantly contribute to forgetfulness, said study co-author Dr. Scott Small, director of the Alzheimer's Disease Research Center at the university, in a press release.
No doubt this is comforting news for anyone who's ever worried that a bout of forgetfulness might be a sign of Alzheimer's.
The study, conducted in postmortem human brain cells and in mice, also offers a major piece of evidence that age-related memory loss and Alzheimer's disease are distinct conditions. The findings were published this week in the online edition of Science Translational Medicine.
"Our study provides compelling evidence that age-related memory loss is a syndrome in its own right, apart from Alzheimer's. In addition to the implications for the study, diagnosis, and treatment of memory disorders, these results have public health consequences," said lead author Dr. Eric R. Kandel.
The hippocampus, a brain region that consists of several interconnected subregions -- each with a distinct neuron population -- plays an important role in memory. Studies have shown that the first region affected by Alzheimer's is often the entorhinal cortex, which is connected to the hippocampus and other regions that are vital for memory. Initially, researchers believed that age-related memory loss is an early manifestation of Alzheimer's, but growing evidence suggests that it is a distinct process impacting a subregion of the hippocampus that receives direct input from the EC.
To determine the role played by RbAp48 in age-related memory loss, the researchers looked at mouse studies. When the researchers genetically inhibited RbAp48 in the brains of healthy young mice, they found the same memory loss as in older mice, as measured by various tests. When RbAp48 inhibition was turned off, the mice's memory became normal again.
The broader point of the research? To identify the right target so that effective interventions can be developed.
"There's been a lot of handwringing over the failures of drug trials based on findings from mouse models of Alzheimer's," Dr. Small said in a press release. "But this is different. Alzheimer's does not occur naturally in the mouse. Here, we've caused age-related memory loss in the mouse, and we've shown it to be relevant to human aging."
A Pew Research study showed that about one-in-four adults ages 65 and older report experiencing memory loss.
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