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November 30, 2020 // -- In a recent study published in the international journal Cell Reports entitled "Cross-Species Analyses Identify Dlgap2 as a Regulator of Age-Cognitive Related and Alzheimer's Dementia," scientists from institutions such as the University of Maine found a gene that helps promote communication between neurons in the nervous system or is directly related to Alzheimer's disease and cognitive decline in the body.
, the researchers revealed genetic molecular mechanisms that affect the body's cognitive decline and dementia tolerance or susceptivity.
After studying the memory and brain tissue of a large number of mice with different genetic characteristics, the researchers found that the expression of the Dlgap2 gene was associated with the extent of memory loss in mice and the risk of Alzheimer's disease in humans, and further research was needed to determine how the gene affected individual dementia and mental function.
Dlgap2 gene, located in neuron synapses, is a key subject for anchoring signals between neurons needed for learning and memory, and when studying brain tissue in post-death humans, the researchers found that people who experienced poor cognitive health and rapid cognitive decline before death tended to have lower levels of the Dlgap2 gene in the body.
Photo Source: Tiffany Laufer researcher Kaczorowski says this is important because many studies around cognitive aging and Alzheimer's disease have focused too much on well-known risk genes such as APOE and brain lesions; now we want to analyze new things that scientists have been ignoring because we've never heard of the Dlgap2 gene before.
researchers found that Dlgap2, which can affect the formation of dendritic spines in neurons, affects the cognitive function of the brain, and in mice, long, thin, mushroom-like ratchet-like structures exhibit higher mental performance, while cognitive decline is directly related to the absence of dendrites. In the
article, the researchers explored how the Dlgap2 gene affects cognitive function in the brain and how it can be used as a treatment for memory loss, especially by using CRISPR gene editing tools to manipulate the gene, and how drugs can be used to regulate the expression of the Dlgap2 gene to help prevent cognitive decline as we age.
Dlgap2 study involved 437 mice, each 6 months, 12 months old or 18 months old.
researchers say this is great because they can take advantage of mouse studies and the best parts of human society, and historically, the researchers have done research in close-family mice with similar genetic make-up, as well as in similar genetic models, but in clinical studies humans don't seem to work that way because they're not genetically identical. In the
article, the researchers analyzed the mouse population's quantitative shape-point mapping and examined the entire genome sequence to identify the genes responsible for different cognitive functions and their unknowns in the sequence, and when the relationship between the Dlgap2 gene and memory loss in mice was determined, the researchers used genome-wide association studies of Alzheimer's disease, as well as imaging, microscopes, and other techniques to study the brain tissue of post-death individuals to assess their significance and importance in human mental function.
researchers say they will continue to conduct more in-depth studies later to understand the link between Alzheimer's disease and the Dlgap2 gene.
() References: Andrew R. Ouellette, Sarah M. Neuner, Logan Dumitrescu, et al. Cross-Species Analyses Identify Dlgap2 as a Regulator of Age-Related Cognitive Decline and Alzheimer's Dementia, Cell Reports (2020). DOI: 10.1016/j.celrep.2020.108091【2】Team discovers new connection between Alzheimer's dementia and Dlgap2by University of Maine。