Researchers at the University of Maryland School of Medicine (UMSOM) provided insights into the mechanisms behind the age-related decline in any memory of personal interactions. The study is published in the journal Aging Cell.
In order to understand the link between social interactions, aging, and memory, the research team sought to determine the role played by an enzyme, known as PDE11A, in the brain area containing memories of social interactions. They studied mouse “social interaction”.
They surveyed the subject mice’s willingness to try new food based on social associative memory. This social associative memory was formed by smelling food on another mouse’s breath or the smell of the other mouse’s pheromones.
The results provided interesting insights into how and why memories decline with age. It revealed that the levels of the PDE11A enzyme increase with age, especially in the hippocampus which stores any memory of personal interactions or learning.
This triggers and accelerates age-related memory loss and cognitive decline associated with social interactions. It was also found that genetically deleting the PDE11A gene helps abate the loss of social associative memory.
Speaking on the possibility of incorporating gene removal therapy in the treatment of memory disorders, one of the lead researchers, Dr. Kelly, elaborated: “PDE11 is involved in more things than just memory. So, if we are to develop a therapy to help with cognitive decline, we [should figure out a way] to target the bad form of PDE11A specifically, in order to not interfere with the normal, healthy function of the enzyme.”
To Know More You May Refer To
Pilarzyk, K., Porcher, L., Capell, W. R., Burbano, S. D., Davis, J., Fisher, J. L., Gorny, N., Petrolle, S., & Kelly, M. P. (2022). Conserved age-related increases in hippocampal PDE11A4 cause unexpected proteinopathies and cognitive decline of social associative memories. Aging cell, e13687. Advance online publication. https://doi.org/10.1111/acel.13687