Restoring Protein Homeostasis Enhances Memory Deficits In Down Syndrome

Restoring Protein Homeostasis Enhances Memory Deficits In Down Syndrome

Down syndrome is the most ordinary genetic factor of intellectual impairment, and presently there is no effective therapy. Memory deficits are a trademark of this case and a research posted this week in the Sciencejournal tells that the defects in a preserved stress pathway named as ISR, or integrated stress response, can clarify the cognitive deficits in Down syndrome’s mouse model.

The authors discovered that ISR is triggered in the mouse model’s brains that sums up the human syndrome’s cognitive deficits and also in samples from patients suffering from postmortem human brain. More essentially, embarrassment of the ISR, either by pharmacological or genetic means, mice suffering from reversed memory deficits. The results support performing future researches to find the odd that modulating the ISR may assist cure Down syndrome and other diseases leading from disturbance of this network.

“In the present research, we probed the role that protein homeostasis networks has in the disease,” claimed Dr. Mauro Costa-Mattioli, corresponding author, to the media in an interview. “A drop in protein homeostasis networks is majorly associated to various neurological cases, from neurodegenerative to aging disorders, but little was recognized about its play in Down syndrome.”

The scientists first found that the protein synthesis rates were lowered in the Down syndrome mice brains and in human cells separated from people suffering from the syndrome. They also discovered that triggering of the ISR, a developing network that manages protein homeostasis by maintaining synthesis of protein, can clarify the deficits of protein synthesis related to Down syndrome.

Encouraged by these motivating results Costa-Mattioli and his team probed if the triggering of the ISR intervened the long-term memory deficits in mice suffering from Down syndrome. To solve this doubt, they employed 4 separate pharmacological and genetic manipulations to fix the ISR in the mouse model for Down syndrome.

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