In BriefAs animals get older, it's normal to see their mental faculties decline. Now, scientists have demonstrated that a single gene has a massive effect on this process.
The Mental Effects of Aging
As animals get older, the electrophysiology of their hippocampal connections begins to degrade. A new study appears to have identified the family of genes that are responsible, demonstrating how a single gene can have a broad effect on age-related decline.
The key component seems to be a protein called FKBP, which is responsible for calcium release within neurons. In the study, rats were injected with viruses engineered to promote overexpression of FKBP1b, and then observed as they attempted to find an underwater platform in a water maze. They were later euthanized so that the researchers could analyze gene expression in their hippocampi.
The rats who received the treatment were found to perform much better than control animals of the same age. What’s more, the hippocampal expression levels of over 800 other genes had been altered as well as the FKBP1b overexpression. The vast majority of these changes caused levels to resemble younger rats more closely than older rats.
Excessive calcium release had already been linked to age-related decline by an earlier study, where increased FKBP expression was seen to increase cognitive function in older rats. The new findings raise further questions, but there are hopes that it could lead to some new ideas in how we respond the mental changes humans experience in old age.
The next step for the researchers involved with this project is to figure out why FKBP levels decrease as animals get older, and what can be done to prevent this from happening. It’s been suggested that metabolic conditions or changes to other cells might be the culprit.
“Another key question is whether Ca2+ dysregulation is why aging is the leading risk factor for Alzheimer’s disease,” wrote the paper’s lead author J.C. Gant in email correspondence with Futurism. “In most neurodegenerative disorders age is a major risk factor and it may be that changes in neuronal calcium are a trigger for multiple diseases. This we do not know, yet.”
Of course, there’s a need for clinical trials to determine whether FKBP expression could be safely manipulated in humans. Gant is hopeful that such trials could take place sooner rather than later, given that we’re already seeing studies using adeno-associated viral vectors to increase gene expression in specific areas of the brain. A microsyringe would be used to inject the virus into the region where it’s needed (in this case the hippocampus).
“Although clinical trials must be run to determine the viability, the debilitating nature of memory loss in normal aging and extreme cases such as Alzheimer’s makes minimally-invasive measures such as this seem more and more viable with respect to alternative consequences of not treating the disease,” explained Gant.
The findings of this study don’t necessarily mean that we have a solution to the way our brains wane as we get older. However, they do offer up some intriguing possibilities when it comes to figuring out what is actually happening inside our bodies that causes this decline to take place.