Researchers at the Centre for Genomic Regulation (CRG) have found that the Snhg11 gene is critical for the function and formation of neurons in the hippocampus. Experiments with mice and human tissues revealed that the gene is less active in brains with Down syndrome, potentially contributing to the memory deficits observed in people living with the condition. The findings are published in the journal Molecular Psychiatry.
Traditionally, much of the focus in genomics has been on protein-coding genes, which in humans constitute around just 2% of the entire genome. The rest is “dark matter,” including vast stretches of non-coding DNA sequences that do not produce proteins but are increasingly recognized for their roles in regulating gene activity, influencing genetic stability, and contributing to complex traits and diseases.
Snhg11 is one gene found in the dark matter. It is a long non-coding RNA, a special type of RNA molecule that is transcribed from DNA but does not encode for a protein. Non-coding RNAs are important regulators of normal biological processes, and their abnormal expression has been previously linked to the development of human diseases, such as cancer. The study is the first evidence that a non-coding RNA plays a critical role in the pathogenesis of Down syndrome.
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