Interesting research was performed by Dr. Natalie Berube’s group from Western University and Lawson Health Research Institute about the role of ATRX gene and its role in brain function and aging. The paper, published in the Journal of Clinical Investigation, tells us the story of premature aging in mice that lack ATRX gene.
Apparently, if we completely switch off this gene, mice will have reduced growth, shortened life span, lordokyphosis, cataracts, heart enlargement, and hypoglycemia, as well as reduction of mineral bone density, trabecular bone content, and subcutaneous fat. These all are signs of premature aging. Researchers found that on molecular level animals with no ATRX gene develop severe damage of telomeres in their brains, specifically in the forebrain and anterior pituitary and reduced levels of thyroxine and IGF-1.
Basically this means that ATRX gene is responsible for maintaining DNA integrity. Less DNA damage – better survival. The animals didn’t have ATRX gene in their brains only, therefore all of the detrimental effects were apparently due to effects of embryonic development. Hence, ATRX must be a crucial protector from DNA damage in proliferating cells.
Here comes the important question – what happens to ATRX activity in humans during aging? Does it remain the same as it is in a young body? It would be interesting to investigate this, because if ATRX activity is lover in older people than in younger ones, then it means that this gene is securing our longevity, apparently by protecting us from DNA damage. In this case, it could be another target for longevity therapy.