Protein that boost long-term memory identified

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Washington, Oct 2 (ANI): Neuroscientists at Cold Spring Harbor Laboratory (CSHL) have discovered a protein that boosts long-term memory in people by controlling their rest intervals.

The study, carried out by researchers led by Dr. Professor Yi Zhong in a fruit fly model, found that the protein, called SHP-2 phosphatase, controls this so-called "spacing effect" by determining how long resting intervals between learning sessions need to last so that long-lasting memories can form.

"Although there are many theories that explain the spacing effect at the psychological level and hundreds of studies that back them up, there has not been any understanding of this phenomenon at the neurobiological level. We have shown for the first time that the spacing effect has a genetic and molecular basis," says Zhong.

They also found that the duration of the resting intervals can be manipulated for achieving better memory by genetically altering SHP-2 phosphatase.

"This ability to exploit the spacing effect's molecular control to enhance memory could be useful in a wide range of settings such as education, advertising, and most importantly, in treating learning and memory disorders," said Zhong.

The researchers focussed on genes that when mutated trigger learning and memory disorders such as Noonan's syndrome- a genetically inherited disease with an incidence rate of 1 in 1000 to 1 in 2000 people.

Over half of Noonan's patients have mutations in a gene called PTP11, which encodes the SHP-2 phosphatase protein.

Unlike other disease-related mutations that shut off protein production or impair protein activity, these PTP11 mutations do the opposite - they boost the activity levels of SHP-2 phosphatase.

To understand how this change impedes long-term memory, the researchers engineered these mutations into a gene in fruit flies called corkscrew that is the functional equivalent of PTP11 in humans.

The mutant flies were taught to avoid certain odours via a training regimen of repeated learning sessions broken up by resting intervals lasting 15 minutes.

But this training regimen, which induces long-term memory in normal flies, failed to work in the mutants because the increased activity of SHP-2 phosphatase disturbed the spacing effect.

Zhong's team found that normally, as each learning period ends, SHP-2 phosphatase activity inside stimulated neurons triggers a wave of biochemical signals, which have to peak and decay before the next learning session can begin.

"The repeated formation and decay of the biochemical signal during each rest interval induces long-term memory," said Zhong.

"These findings suggest that SHP-2 phosphatase acts as a molecular timer that determines how long resting intervals should last

"Our results suggest that longer resting intervals for Noonan's patients might reverse their memory deficits," he added.

The study has been published online in the journal Cell. (ANI)

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