Restoring Process In A Gene Altering In Down Syndrome Seen In Mouse

The research study showing that the restoring process in a gene altering in Down syndrome; rescues the adult neurogenesis and learning and memory defects in mice. Where the researchers explaining the restoring a gene altered in Down syndrome called the Down syndrome critical region 1 (DSCR1) rescued adult neurogenesis and learning and memory defects in a Down syndrome mouse model (Ts65Dn).

In this procedure describing the restoring a gene altering in the Down syndrome called the Down syndrome critical region 1 (DSCR1) rescued adult neurogenesis and learning and memory defects in a Down syndrome mouse model (Ts65Dn). These results highlight that DSCR1 contributes to intellectual disability in Down syndrome, and further pave the way for treatment. But as adult neurogenesis is the process of generating new neurons in the adult brain.

Gene altering in Down syndrome

Defects in adult hippocampal neurogenesis have been observing in various animal models of neurological disorders; including schizophrenia, depression, Parkinson’s disease, Alzheimer’s disease, and neurodevelopmental disorders such as Down syndrome. However, the precise cellular and molecular mechanisms underlying adult hippocampal neurogenesis; and their links to neurological disorders are not well understood.

However, discovering that DSCR1 is required for adult hippocampal neurogenesis, and furthermore elucidated mechanisms underlying how DSCR1 regulates this process. They showed that DSCR1 binds to and modulates TET1 splicing, which subsequently controls miRNA-124 expression by regulating the methylation status of the miRNA-124 promoter. Loss of DSCR1 leads to increase TET1 levels, resulting in miRNA-124 promoter hypomethylation and increased miRNA-124 expression. But the DSCR1 transgenic mice display opposite changes; albeit they also have defects in adult hippocampal neurogenesis.

Hippocampal neurogenesis

Strikingly, correcting DSCR1 dosage alleviates both the impaired adult hippocampal neurogenesis and the defective learning and memory seen in a Down syndrome mouse model (Ts65Dn). Together, the results reveal that precise regulation of DSCR1 and the interplay between TET1 and miRNA-124 are crucial for normal adult hippocampal neurogenesis. These findings further highlight potential therapeutic targets for the treatment of Down syndrome and other neurological disorders associated with adult neurogenesis.

The expression of two epigenetic regulators; mediated by the DSCR1 protein, is important for regulating adult neurogenesis in the hippocampus. This is likely a key mechanism contributing to defective adult neurogenesis observed in the Down syndrome mouse model. The findings not only provide a basic understanding of the mechanisms regulating adult hippocampal neurogenesis; but will also contribute to the development of a novel therapy for the cognitive deficits manifested in Down syndrome patients.