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    Home > Biochemistry News > Biotechnology News > Aging Cell: How interpersonal memories decay with age

    Aging Cell: How interpersonal memories decay with age

    • Last Update: 2022-09-21
    • Source: Internet
    • Author: User
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    Figure: PDE11A memory enzyme (green) in the brains of young (left) and elderly (right)
    mice.

    Image credit: University of Maryland School of Medicine

    One of the most frustrating aspects of age-related memory decline is that you can't remember the faces
    that accompany the names of people you talked to hours ago.
    While researchers don't yet know why this dysfunction occurs, a new study conducted by the University of Maryland School of Medicine (UMSOM) offers some important new clues
    .
    The study was published Sept.
    8 in the journal Senescent Cells
    .

    By studying aging mice, the researchers discovered a new mechanism in neurons that causes memories associated with these social interactions to decline
    with age.
    In addition, they were able to reverse this memory loss
    in the lab.

    The researchers report that their findings identify a specific goal in the brain that could be used in the future to develop treatments to prevent or reverse memory loss
    due to typical aging.
    Aging memory problems are different
    from memory problems caused by diseases such as Alzheimer's or dementia.
    Currently, there are no drugs that can prevent or reverse the cognitive decline
    caused by typical aging.

    Dr Mitch Kelly, head of the study and associate professor of anatomy and neurobiology at UMSOM, said: "If an elderly person attends a cocktail party, they are likely to recognize the names or faces of other participants afterwards, but they may have a hard time remembering which name corresponds to
    which face.
    "

    This kind of memory, which correlates multiple pieces of information in interpersonal interactions, is called socially associated memory and requires an enzyme called PDE11A, located in the part of the brain responsible for the memory of life experiences
    .
    Last year, Dr.
    Kelly published a study on PDE11A that showed that mice with similar PDE11 enzyme genes were more likely to interact
    than mice with different PDE11A genes.
    In the new study, Dr.
    Kelly and her team sought to determine the role of PDE11A in social associative memory in aging brains, and whether this memory loss
    could be prevented by manipulating the enzyme.

    Researchers can study rats' "social interactions" with their neighbors by observing whether they are willing to try a new food, based on their memories
    of encountering it during another mouse's breath.
    Rats don't like to eat new food to avoid getting sick or even dying
    .
    When rats smell the smell of food from the breath of another mouse, they associate the smell of food with the smell of another mouse's pheromone, and the memory of the pheromone serves as a safety signal that any food with this smell can be safely eaten
    in the future.

    Dr.
    Kelly and her colleagues found that while older mice were able to recognize food odors and social odors, respectively, they were unable to remember the link between the two, similar
    to cognitive decline in older adults.

    They also found that PDE11A levels in humans and mice increased with age, particularly in areas of the brain responsible for multiple kinds of learning and memory, the hippocampus
    .
    Additional PDE11A in the hippocampus is not only found in normal locations in juvenile mice; Instead, it preferentially gathers in the form of filaments in the compartments of neurons
    .

    The researchers wondered if the filaments contained too much PDE11A, and whether that was why
    the older mice forgot their social association memories and stopped eating the safe food they smelled in other mice' breaths.
    To answer this question, they prevented these age-related increases
    in PDE11A by genetically deleting the PDE11A gene from mice.
    Without PDE11A, older mice no longer forget social association memories, meaning they eat safe food
    that smells the breath of another mouse.
    When the researchers re-injected PDE11A into the hippocampus of these elderly mice, the mice again forgot their social association memories and stopped eating safe foods
    .

    The researchers found that the concentrated PDE11A filaments had an additional chemical modification at a specific location in one enzyme, while another PDE11, which was scattered throughout the neuron, did not
    .
    When they prevented this chemical modification, they lowered the level of PDE11 and also prevented it from accumulating in the form of filaments
    .

    "PDE11 has a lot more to do with memory, including preferences
    about who you like to be with.
    So, if we're going to develop a treatment to help with cognitive decline, we don't want to get rid of it entirely, otherwise it could lead to other negative side effects
    .
    "She jokes with her colleagues that any medication to eliminate PDE11 will make sure you remember your friends and family, but you may no longer like them
    .
    " Therefore, our goal is to find a way to specifically target the undesirable form of PDE11A so as not to interfere with the normal, healthy function of
    the enzyme.

    Dean Mark T.
    Gladwin, MD, executive vice president of medical affairs at UM Baltimore and Distinguished Professors John Z.
    and Akiko K.
    Bowers of UMSOM, said, "We're just the tip of the iceberg when we understand how the brain ages, so it's critical to have such basic research to help us learn more and ultimately find ways
    to prevent cognitive decline.
    "

    Other authors of the study include UMSOM students Nicole Gorny and Siena Petrole, and co-authors
    from the University of South Carolina.

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