A new research team at the University of Maine discovered a facilitative communication between an existing gene called Dlgap2 and Alzheimer’s dementia. It was uncovered that Dlgap2 that facilitates communication between neurons in the nervous system, is found to be associated with the degree of memory loss in mice and risk for Alzheimer’s dementia in humans.
Researchers while examining the post-mortem human brain tissue, discovered low levels of Dlgap2 in people who experienced poorer cognitive health as well as faster cognitive decline in their lifetime, with research findings of the study published in the journal Cell Reports.
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Aging is one of the leading risk factors for numerous cognitive or nervous system disorders, including dementia in Alzheimer’s disease. Accumulating evidence give elucidative mechanism underlying ageing process, yet they fail to explain the cognitive aspects. According to researchers, it is believed that genetics play a critical role in identifying a person’s susceptibility or resilience to cognitive decline and dementia.
In the study, researchers used a mouse model because it clearly represents a critical resource to identify genetic factors influencing complex traits.
Nearly forty million people have Alzheimer’s or dementia today. We have no way to stop or even slow the disease at this point, but I’m hopeful the new Alzheimer’s Disease Data Initiative (@AlzData) will speed up progress. https://t.co/O5vXNkghFK
— Bill Gates (@BillGates) November 17, 2020
In this large-scale study, researchers did a cross-sectional evaluation of cognitive performance in the mouse model aged 6 to 18 months. They identified a single protein-coding positional candidate named Dlgap2, that was most likely mediating age-related memory decline.
It was found that Dlgap2 is a critical component of spine, mostly influences spine region, and is found to significantly correlates with cognitive outcomes. Notably, the research team, after elucidating the memory and brain tissue from a large group of genetically diverse mice, they found that the Dlgap2 gene expression is believed to be associated with the memory decline and Alzheimer’s dementia (AD) in diverse human populations.
However, further research will be required to ascertain how the gene influences dementia as well as mental function.
Dlgap2 gene is situated in the synapses of neurons where they serve to anchor critical receptors for signals between neurons required for learning and memory. The current study helps in intervening new research opportunities for additional research into Dlgap2.
Andrew Ouellette, a Ph.D student at JAX and a GSBSE NIH T32 predoctoral awardee, led the project, along with his mentor Kaczorowski and scientists from across the U.S. says they he plans to explore the mechanisms how Dlgap2 influences thought and reasoning, and how it can be used for therapeutic purposes for memory loss, partly by manipulating the Dlgap2 gene by editing CRISPR tool.
Whereas other team members of the Kaczorowski lab are currently studying how with pharmaceutical help, Dlgap2 can be regulated to cognitive decline with age.