Science

Scientists reverse Down’s syndrome learning deficiency in mouse

A new study done by researchers from the University of California, San Francisco and Baylor College of medicine could offer hope in reversing the symptoms associated with Down’s syndrome in humans as they were able to replicate this process in mice where they were able to reverse the learning and memory deficits in them.

Down’s syndrome is usually associated with an altered protein production in the hippocampus area and by administering drugs that can target the body’s response to stresses at the cellular level, they were able to bring back the normal production of protein, which is then found to obviate and restore the cognitive impairments.

The usual approach for Down’s syndrome is studying the genes in the extra chromosome 21 and its related pathologies however their new approach tries to uncover the link between protein regulation, known as proteostasis, and Down’s syndrome, according to Peter Walter, professor of Biochemistry and Biophysics at UCSF and co-senior author of the study.

They were able to glean that in mice with Down’s syndrome, protein production -got impacted by 39% in the hippocampus area which led to the question of why the extra copy of the chromosome 21 would result in less protein production and found that the extra chromosome was triggering a stress response that limited protein production, which is actually a protective response that gets activated when something is off.

According to Walter, a cell has an inherent capability of monitoring its own health and as a response to unconducive environments, it limits the protein production however as this is a limiting factor for higher cognitive and mental faculties, the individuals have trouble with learning and forming memory as exhibited in patients with Down’s syndrome.

With this new epistemic arsenal, they were able to block the enzyme responsible for the production of stress, PKR, and were able to restore the protein levels and consequently reverse the cognitive impairments in mice.

This new research does provide hope that this could potentially be translated into humans as well.

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