Age-Related Memory Loss and Alzheimer's

In the previous series on stereotypes, I wrote a post about how old people "have" poor memory issues only because they subconsciously reinforce that generalization imposed by society. From what I researched, it seemed that the idea that old people and poor memory are closely related should be considered specious, but I recently stumbled upon an article in the Scientific American about a particular gene in the human brain called RbAp48, whose decrease in amount apparently corresponds, according to Columbia University neuropsychiatrist Eric Kandel, with atrophied memories in aged people. While this seems to be somewhat of a contradiction, the article has many valuable points on what implications that the discovery of this memory-related gene may have in the future for aged people.

To first describe the research, Kandel’s intention in his study was to search for a method that effectively differentiates between age-related memory loss and Alzheimer’s Disease, which both materialize in the hippocampus--the human brain’s memory factory and storage facility--and share numerous early symptoms. The similarities sometimes causes people to not consider the two afflictions as separate. However, one clear difference that Kandel and other researchers discovered was that RbAp48 levels in people with age-related memory loss changed noticeably while people with Alzheimer’s experienced almost no alterations in those levels. This seems to be correlated with the fact that brain cells affected by age-related memory loss are just “sick” or “offline” and therefore have less RbAp48 levels than normal.

Kandel’s research partner, director of Alzheimer’s research at Columbia named Scott Small, posits that the reintroduction of RbAp48 at specific loci in the human brain may lead to the reversal of age-related memory loss. With more tests and research, pharmaceuticals containing the gene may be distributed for aging people with poor memory levels in the future. However, as wonderful as curing age-related memory loss seems, one main issue still remains: how to cure Alzheimer’s Disease. Unlike memory loss, Alzheimer’s permanently eliminates brain cells rather than make them “sick,” and the RbAp48 “treatment” would not work simply because the disease does not seem to be related to amounts of the gene. Another question that leaves from the Columbia researchers’ work is why the RbAp48 levels decrease in age-related memory loss and not in Alzheimer’s. It’s hard to note whether the knowledge of this gene’s role in natural memory loss may be a key step in perhaps understanding Alzheimer’s more or may be a red herring that distracts researchers from looking for other explanations.