[Science Solitaire] The suspect gene behind ‘senior moments’

Maria Isabel Garcia
What is it about age that gets us 'stuck' when trying to recall a name, a location?

There is a line in a song I like that goes: “And time weaves ribbons of memories to sweeten life when youth is through.” But we all know that time is also notorious for doing the opposite – for letting loose many of the knotted gems (and junk) we have stored in our heads where often they end up never to be retrieved again. 

Are senior moments necessarily tied to age? What is it about age that gets us “stuck” when trying to recall a name, a location? What do young people have in their brains that prevent them from having “senior moments”?  And are these senior moments a foreshadowing of the dreaded “A” (Alzheimer’s disease) where your identity fades away even from your own self?   

A study made by a Nobel prize-winning neurobiologist Eric Kandel, 84, and his colleagues from Columbia University was published last Aug 28 in the journal Science Translational Medicine. They thought they have found an important gene that is responsible for age-related memory loss.  The title of the study is “Molecular Mechanism for Age-Related Memory Loss: The Histone-Binding Protein RbAp48.”

I also listened to NPR’s Ira Flatow as he interviewed Erik Kandel about these new exciting findings and what it could possibly mean for aging and memory.

The study was reassuring because it found that the pathology of Alzheimer’s is different from the memory glitches that we experience as we age.  This should lessen our fear that as we age and start to forget someone’s name or where we placed the TV remote, it already necessarily means we are on our way to having Alzheimer’s.

Gene that strengthens memory

In previous studies, it was shown that Alzheimer’s begins in a part of the cortex called the entorhinal cortex; while age-related memory loss starts in the dentate gyrus – part of the hippocampus which is strongly associated with memory.  So Kandel and his colleagues focused on this difference and compared the brains of deceased people ages between 38 and 90. They compared their entorhinal cortext and dentate gyrus. What they found was a gene that reliably declined as the brain got older and this was gene RbAp48.

SUSPECT GENE. A study reveals that the pathology of Alzheimer’s is different from the memory glitches that we experience as we age. Image by Shutterstock

Then they wanted to check what it would do to living organisms. Since injecting these in humans was out of the question (yet), they turned to mice.

They knocked off that gene in young mice (3 months old) and they have observed that those young mice showed poor memory. But they boosted that same gene in old mice and it resulted in memory that was shown to be as good as new.  They did this by exposing mice to objects (one new to the mice and one that is not new to the mice). 

Mice take a longer time to look at a new thing so that when mice took equal or longer with an old thing then it means that those mice do not remember having seen it before.

This clearly showed that first, RbAp48 is an important gene in strengthening and storing memory; second, that it really degrades with age; and third, it is not the same Alzheimer’s which is associated with beta amyloid (plaque) accumulation.

Can template of aging be decoded?

But what makes the gene decline with age? They really do not know yet. All they know is it does. The scientists also suspect that it is not a lone actor in memory-making. They think it acts in conjunction or in a cascade with other genes that turn on or off so they will keep on looking. 

Kandel was quick to warn that you cannot just take the protein this gene does and boom, you have memory that is consistently robust. He emphasized that there is no such pill available, yet. Also, he said that taking a pill orally is not often the most reliable way of delivering these kinds of proteins to your brain since proteins digest very fast and there may be little or none left after digestion to be delivered to your brain. 

He says it is also possible that what the gene does in terms of boosting memory, or at least your ability to think better, could also be helped or triggered by other activities as studies have shown like exercise.

Before this golden age of neuroscience where we could now peer into living brains and even inject them with our suspect genes, we thought the template of aging could never be decoded.  But as continuing studies reveal how we make, store and retrieve memories, science may one day come out with ways to reverse the dialogue on aging.  If the older folks would be able to remember and learn as much as the younger ones, with experience working to the former’s advantage, what would the world look like in terms of its schools and workforce?

And if we are able to reverse age-related memory loss in older folks, what about the fate of our aging and therefore weakening muscles and bones?  Would youth one day be the permanent status of the living?  Would it be possible that to grow old will one day be an option and not our common fate? – Rappler.com

Maria Isabel Garcia is a science writer. She has written two books, “Science Solitaire” and “Twenty One Grams of Spirit and Seven Ounces of Desire”.  Her column appears every Friday and you can reach her at sciencesolitaire@gmail.com


DNA image by Shutterstock

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