Home Health A new study shows how memory for personal interactions deteriorates with age

A new study shows how memory for personal interactions deteriorates with age

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The memory enzyme PDE11A (green) in the brains of young (left) and old (right) mice. Credit: University of Maryland School of Medicine

One of the most frustrating aspects of age-related memory loss is not being able to remember the face that accompanies the name of someone you just talked to a few hours ago. Although researchers do not understand why this dysfunction occurs, a new study conducted at the University of Maryland School of Medicine (UMSOM) has provided some important new clues. The study was published on September 8 in Cell aging.

Use aging mice, researchers have identified a new mechanism in neurons that causes memories associated with these social interactions to deteriorate with age. Also, they were able to undo it memory loss in the laboratory.

The researchers report that their findings have identified a specific target in the brain that could one day be used to develop treatments that could prevent or reverse memory loss due to typical aging. Older memory problems are different from problems caused by diseases such as Alzheimer’s or dementia. Currently, there are no drugs that can prevent or reverse the decline in cognitive function due to typical aging.

“When an older person comes to a cocktail party, they are more likely to recognize the names or faces of the other participants afterward, but they may have difficulty remembering which name goes with which face,” said study leader Michie Kelly, Ph.D. ., Associate Professor of Anatomy and Neurobiology at UMSOM.

These kinds of memories, which link multiple pieces of information in a personal interaction, so-called social associative memories, require an enzyme known as PDE11A in the part of the brain responsible for remembering life experiences. Last year, Dr. Kelly published research on PDE11A showing that mice with genetically similar versions of the PDE11 enzyme are more likely to interact than mice with a different type of PDE11A. In this new study, Dr. Kelly and her team sought to determine the role of PDE11A in social associative memory in the aging brain and whether manipulation of this enzyme could be used to prevent memory loss.

Researchers can study mice’s “social interaction” with their neighbors, seeing if they’ll want to try a new food based on their memories of encountering that food on another mouse’s breath. Mice do not like to eat new food in order not to get sick or even die. When they smell food on another mouse’s breath, the mice make an association between the food smell and the other mouse’s pheromone smell, the memory of which serves as a safety signal that any food with that smell is safe to eat in the future.

Dr. Kelly and her colleagues found that while old mice could recognize both food and social odors separately, they were unable to remember the association between them, similar to cognitive decline in elderly people.

They also found that levels of PDE11A increased with age in both humans and mice, particularly in an area of ​​the brain responsible for many types of learning and memory, known as the hippocampus. This extra PDE11A in the hippocampus was not simply found where it would normally be found in young mice; instead, it preferentially accumulated as small filaments in neuronal compartments.

The researchers wondered if too much PDE11A in these filaments was the reason the older mice forgot their social associative memories and will no longer eat safe food that they smelled on another mouse’s breath. To answer this question, they prevented the age-related increase in PDE11A by genetically deleting the PDE11A gene in mice. Without PDE11A, old mice no longer forgot social associative memory, meaning they ate safe food that smelled like another mouse’s breath. When the researchers added PDE11A back into the hippocampus of these old mice, the mice once again forgot the social associative memory and stopped eating the safe food.

One potential path to developing drugs to prevent this memory loss in humans lies in an additional discovery: The researchers learned that the concentrated strands of PDE11A had an additional chemical modification at a specific site on the enzyme that the other PDE11, which was distributed throughout neurons, did not. to have When they prevented this chemical modification, it reduced PDE11 levels and also prevented it from accumulating as filaments.

“PDE11 is involved in more things than just memory, including preferences for who you prefer to be around. So if we want to develop a therapy to help with cognitive decline, we don’t want to get rid of it completely or it could cause other negative side effects,” said Dr. Kelly. She and her colleagues joke that any drug that that eliminates PDE11 ensures that you remember your friends and family, but you may no longer like them.” So our goal is to figure out how to specifically target the bad form of PDE11A so it doesn’t interfere with normal , healthy function enzyme.”

Dean Mark T. Gladwin, MD, executive vice president for medical affairs at the University of Baltimore and the John Z. and Akiko K. Bauer Distinguished Professor at UMSOM, said, “We are at the tip of the iceberg when it comes to understanding as the brain ages, so it’s vital that basic research like this is done to help us deepen our understanding and ultimately find ways to prevent cognitive decline.”

Additional study authors include students Nicole Gorney, M.S., and Sienna Petrole of UMSOM, along with co-authors from the University of South Carolina.



Additional information:
Kathy Pilarczyk et al. A persistent age-related increase in PDE11A4 in the hippocampus causes unexpected proteinopathies and cognitive decline in social associative memories, Cell aging (2022). DOI: 10.1111/acel.13687

Citation: New study identifies how memory of personal interactions declines with age (2022, September 8) Retrieved September 8, 2022 from https://medicalxpress.com/news/2022-09-memory-personal-interactions-declines- age.html

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