Exactly how RbAp48 does that is not clear. The protein acts as a sort of genetic master key: By causing chromosomes to loosen their hold on the molecular spool they are wound around like thread, it allows genes to be turned on. Among the activated genes, Kandel explained, are those involved in forming memories.
The emerging picture is that levels of RbAp48 decline with age, allowing chromosomes to maintain a death grip on their spools. Memory genes remain dormant, and you can’t remember that you promised your spouse you would make dinner.
The researchers plan to see what social and dietary factors might boost RbAp48 in mice, said Kandel, who will be 84 in November. Pharmaceuticals, nutraceuticals, physical and cognitive exercise are all candidates, said Columbia’s Dr Scott Small, co-senior author of the study.
Testing such interventions in mice should be more useful to humans than tests of drugs for Alzheimer’s, he said. RbAp48 “is different,” Small said. “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.”
(Reporting by Sharon Begley; Editing by Julie Steenhuysen and Prudence Crowther)
Article Appeared @http://www.reuters.com/article/2013/08/28/us-science-memory-idUSBRE97R12A20130828