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
The study has just been published in the journal Nature
Neuroscience and received a 2 million euro grant from the European Research
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
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
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
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.
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
They managed to show that a non-genetic factor affects the
structure of the presenilin and the formation of amyloid-beta.
significant, Slutsky explained, as it is a major step in identifying factors
that cause the sporadic type that affects million of people around the
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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