Evidence Points to Proteins in Age-Related Memory Loss

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Studies on mice reveal a link between decreased production of a particular protein and memory problems. That’s according to research at Columbia University which offers hope for progress in our understanding of age-related cognitive decline in humans.

Evidence has accumulated for some time about the crucial role certain proteins play in memory formation and retention. There’s also abundant evidence that certain regions in the brain (most notably, particular areas of the hippocampus) are heavily involved in both forming and retaining memories. Now, a study conducted by a team of researchers at Columbia University and published in the journal Science Translational Medicine suggests that one particular protein may play a key role in the difficulties many elderly individuals — even those not afflicted with Alzheimer’s Disease or other types of dementia — experience with forgetfulness and learning new things.

As we age, certain physiological changes in our brains are inevitable. For example, we lose brain cells. Fortunately, our brains are endowed with such a plethora of neurons to start with that losing a few of them over time is something we barely notice. But as we age, and with other typical assaults on our brain cells, the rate of loss speeds and can eventually significantly affect our overall cognitive ability. But some individuals, even though they don’t suffer from a disease process like Alzheimer’s, experience an even higher degree of difficulty remembering things they have long known or learning new things than is considered normal. And now there’s evidence that deficiency in a histone-binding protein called RbAp48 might be the culprit.

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Age-related cognitive decline is very different from Alzheimer’s Disease and other types of dementia. It’s memory impairment in excess of what’s typical for aging, but it doesn’t share the same etiology or prognosis of the other dementias. Proteins do seem to be involved in both Alzheimer’s and age-related cognitive decline. But in Alzheimer’s, the principal culprit appears to be the formation of “plaques” that interfere with the communication process between neurons, whereas in age-related cognitive decline, the difficulty appears to center around reduced protein production and changes in the dentate gyrus section of the hippocampus.

The Columbia researchers had conducted earlier research that strongly pointed to changes in a particular region of the hippocampus — the dentate gyrus, known to be highly associate with memory formation and retention — as well the role of 17 different genes in the formation and expression of various proteins (the most significant of which was RbAp48) as the dominant players in age-related cognitive decline. So they constructed an experiment using laboratory mice with genetic modifications that caused them to produce less of this vital protein. And what they found was that mice producing less of the protein had greater difficulty both retaining information and forming new memories compared to mice with normal levels of the protein. Moreover, mice modified to produce increased levels of the protein performed better on the tests requiring good memory. The improvement in performance was even seen in older mice, who performed as well as younger counterparts. They also found, after examining images derived from magnetic resonance imaging (MRI), that changes occurred in the dentate gyrus area of the hippocampus — the area long known to be crucial to memory formation and retention and also prone to significant change due to aging — in the protein-deficient mice. They concluded, therefore, that decreased production of RbAp48 might very well be linked both to changes in the hippocampal region of the brain critical to memory and to the decline in cognitive abilities older individuals who are not suffering from Alzheimer’s or other types of dementia experience.

While the Columbia study doesn’t signal that a cure for age-related cognitive decline is right around the corner, it does provide promise that some novel new treatment strategies may soon on the horizon. If in fact the reduced production of RbAp48 is the main catalyst for changes in the brain involved in cognitive decline, especially in the regions of the hippocampus strongly associated with memory formation, then devising strategies to boost its levels in the brain might well be the key to staving off memory problems in the elderly not afflicted with more serious memory-robbing diseases. And while the evidence we have for the vital role of this protein presently comes from research using laboratory animals, it will likely not be long before we know more its role in human memory formation and retention.

All clinical material on this site is peer reviewed by one or more clinical psychologists or other qualified mental health professionals. This specific article was originally published by on and was last reviewed or updated by Dr Greg Mulhauser, Managing Editor on .

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