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Published on: December 28, 2014
by The Jerusalem Post:
University of Haifa researchers have found a way to improve memory by suppressing a molecule that is known to function poorly in old age and is closely linked to Alzheimer’s disease. Prof. Kobi Rosenblum in the Sagol department of neurobiology and colleagues recently reported their work in the Journal of Neuroscience.
They reported finding a way to improve memory by manipulating the specific molecule. The researchers even succeeded, for the first time, in manipulating the molecule’s operations without creating any cognitive impairment.
“We know that in Alzheimer’s disease, this protein (known as PERK) doesn’t function properly. Our success in manipulating its expression without causing any harm to the proper functioning of the brain paves the way for improving memory and perhaps even slowing the pathological development of diseases like Alzheimer’s,” said Rosenblum.
Previous studies at the university and other labs throughout the world had shown that the brain’s process of formulating memory is linked to the synthesis of proteins. High rates of protein production will lead to a strong memory retained over the long term, while a slow rate of protein production leads to weak memories that are less likely to be etched into longterm memory.
In the current study, the researchers, Dr. Hadile Ounallah-Saad and Dr. Vijendra Sharma, who work in Rosenblum’s lab sought to examine the activity of a protein called elF2 alpha, a protein known as the “spigot” or regulator that determines the pace of protein synthesis in the brain during memory formation.
From earlier studies, they knew that there are three main molecules that act on the protein and either make it work or stop it from working. During the first stage they sought to determine the relative importance and the task of each one of the molecules that control the activity of efF2 alpha and as a result, the ability to create memories. After doing tests at the tissue and cell levels, the researchers discovered that the main molecule controlling the efF2 alpha’s activity was the PERK molecule.
“The fact that we identified the PERK as the primary controller had particular significance,” said Dr.
Ounallah-Saad. “First, of course, we had identified the dominant component. Secondly, from previous studies we already knew that in degenerative diseases like Alzheimer’s, PERK performs deficiently. Third, PERK acts on various cells, including neurons, as a monitor and controller of metabolic stress. In other words, we found a molecule that has a major impact on the process of creating and formulating memory, and which we know performs deficiently in people with Alzheimer’s disease.”
With this study, they concluded, “we proved we are capable of strengthening the process of protein synthesis in the brain and of creating stronger memories that last a long time.”
“The moment we did this by manipulating a molecule that we know performs deficiently in people with Alzheimer’s and is linked to the aging process, we paved the way for the possible development of drugs that can slow the progress of incurable diseases like degenerative brain conditions, Alzheimer’s chief among them.”
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