Learning and memory impairments in a Down syndrome mouse model were reversed by correcting expression of a gene that influences the generation of new neurons in the brain. The finding could pave the way to treat the cognitive impairment associated with the syndrome in humans.
Adult neurogenesis is the process of generating new neurons in the adult brain. Defects in this process have been observed in various animal models of neurological disorders including schizophrenia, depression, Parkinson’s disease, Alzheimer’s disease, and neurodevelopmental disorders such as Down syndrome. But the precise cellular and molecular mechanisms underlying adult neurogenesis and their links to neurological disorders are not well understood.
Molecular neurobiologist Kyung-Tai Min at Korea’s Ulsan National Institute of Science and Technology and his colleagues found that interactions between a gene called the Down syndrome critical region 1 (DSCR1) and two other molecules, TET1 and miRNA-124, were necessary for adult neurogenesis and were important in learning and memory.