TAU research cause of Alzheimer’s disease

The study has just been published in the journal Nature Neuroscience and received a 2 million euro grant.

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April 14, 2013 03:12
3 minute read.
DR. INA SLUTSKY (center) with Hila Fogel (left) and Dr. Yiftah Dolev.

Dr. Ina Slutsky 370. (photo credit: courtesy)

A new research study at Tel Aviv University hypothesizes that interference with brain activity at high frequency is liable to be the main cause of Alzheimer’s disease.

The study has just been published in the journal Nature Neuroscience and received a 2 million euro grant from the European Research Council.

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There is as yet no cure for Alzheimer’s, which affects an estimated 100,000 Israelis. For over a decade, all attempts to develop drugs for preventing the decline of memory loss have failed, said Dr. Ina Slutsky, head of the research group on synaptic plasticity at TAU’s Sackler Faculty of Medicine and Sagol School of Neuroscience.

“The field is surely ripe for new research directions, and I believe that the answers will be found in basic processes that occur in the brain,” she said.

Slutsky’s lab deals with basic science, meaning research that is far from being implemented into practical use. Three years ago, she discovered the physiological function of the amyloidbeta protein, which is the main component in the plaques found in the brains of Alzheimer’s patients. More recently, the group exposed the physiological processes that regulate the composition of the protein. The researchers believe these new findings will make it possible to identify – many years before the symptoms appear – what initially goes wrong in the brains of people who will develop this type of dementia.

The research, supervised by Slutsky, was led by post-doctoral student Yiftah Dolev and research student Hila Fogel.

Until now, Alzheimer’s researchers around the world focused on a rare genetic condition that occurs already in patients’ 40s rather than in their older years.

They managed to discover 150 genetic mutations that cause the disease, most of which involve two proteins – amyloid precursor protein (APP), from which amyloid-beta is made, and presenilin, which is involved in the final “cut” of the APP before amyloid-beta is produced.

The search for a medication dealt mainly with ways to minimize toxic forms of amyloid, but it did not succeed.

Unlike the early-onset, familial Alzheimer’s that most researchers studied, the common form is sporadic Alzheimer’s, which appears in the last decades of life and causes dementia in 99 percent of sufferers in the world.

Slutsky, aiming at finding the cause of the sporadic type, decided to study the connection between the activity of nerve networks in the brain and the components of amyloid-beta created in brain cells.

The amyloid-beta molecules that form in the brain come in a number of sizes, from 39 to 43 amino acids, Slutsky said. The shorter ones are more common than the longer ones, which produce the plaques. About 100 mutations connected to familial Alzheimer’s disrupt the balance between the two types of amyloid and cause the longer type to be the majority. This is the beginning of the disease. The question was what causes the disruption in the sporadic form of the disease in which people don’t carry familial mutations.

The researchers studied the question by giving electric stimulation to the hippocampus, the part of the brain involved in forming memories, in healthy rats and found that high-frequency “bursts” caused the production of shorter molecules.

They managed to show that a non-genetic factor affects the structure of the presenilin and the formation of amyloid-beta.

This was significant, Slutsky explained, as it is a major step in identifying factors that cause the sporadic type that affects million of people around the world.

The research, she said, is likely in the future to lead to a breakthrough in practical research aimed at finding ways to diagnose, prevent and cure the disease.


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