Alzheimer’s Cure Is Possible Thanks To Synapse Discovery

Posted: Nov 30 2015, 4:59am CST | by , in News | Latest Science News

Alzheimer’s Cure is Possible Thanks to Synapse Discovery
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  • Alzheimer’s Disease may soon be a Thing of the Past

According to scientists, a new discovery of a synapse protein may soon lead to Alzheimer’s disease being a thing of the past.

It has recently become common knowledge that the links between brain cells are obliterated during the onset of Alzheimer’s disease. UNSW Australia scientists lead the team of researchers who discovered this fact.

This has paved the way for a range of cures on a hypothetical level. The vanishing of synapses is the first stage of Alzheimer’s. These synapses connect various neurons in the human brain. They are a necessity for learning purposes and the formation of memory. In fact, all brain functions are dependent on these synapses.

“One of the first signs of Alzheimer’s disease is the loss of synapses – the structures that connect neurons in the brain,” says study leader, Dr Vladimir Sytnyk, of the UNSW School of Biotechnology and Biomolecular Sciences.

“Synapses are required for all brain functions, and particularly for learning and forming memories. In Alzheimer’s disease, this loss of synapses occurs very early on, when people still only have mild cognitive impairment, and long before the nerve cells themselves die.

“We have identified a new molecular mechanism which directly contributes to this synapse loss – a discovery we hope could eventually lead to earlier diagnosis of the disease and new treatments.”

In the earlier stages of Alzheimer’s, the victims only have a little bit of cognitive damage. It is a long and painful journey from this relatively benign stage to the devastating period when all nerve cells simply die off.

A novel molecular mechanism has been found whereby the synapses get wiped out in the first place. It is hoped that this discovery will help in finding a suitable cure for the dreaded malady. Care is better than cure and so an earlier diagnosis is of the essence. And suitable therapeutic steps may be instituted that will work on a regular basis.

A protein termed neural cell adhesion molecule 2 (NCAM2) was thoroughly studied by the experts. This protein is said to help in the formation of synapses. It facilitates the various connections in the brain.

Thus it could prove very useful in the fight against Alzheimer’s. Post-mortem brain samples from people with Alzheimer’s proved that levels of NCAM2 were low in the hippocampus.

Furthermore, this protein is broken up by another protein which is called beta-amyloid. Beta-amyloid is a major part of the plaques that accumulate in the brains of Alzheimer’s patients.

“Our research shows the loss of synapses is linked to the loss of NCAM2 as a result of the toxic effects of beta-amyloid,” says Dr Sytnyk. “It opens up a new avenue for research on possible treatments that can prevent the destruction of NCAM2 in the brain.”

The wearing away of synapses is due to the obliteration of NCAM2 and this in turn is due to the derangements wrought by the protein known as beta-amyloid. The avenues opened up for future research will explore the prevention of NCAM2 destruction.

This is the only direction that holds promise so far. And it just might be the sole means of ending the disease in the times which are yet to come. Alzheimer’s often begins in the ripe years of most senior citizens.

And it progresses steadily to reduce the afflicted person’s memory till all functions necessary for a responsible life are gone. The final stage leads to certain death. It is a degenerative disease of modern civilization and requires new solutions rather than the tried and tested therapeutic methods of yore.

he study’s first author is Dr Iryna Leshchyns’ka of the UNSW School of Biotechnology and Biomolecular Sciences and the team includes researchers from Neuroscience Research Australia and the Dementia Research Unit of the UNSW School of Medical Sciences.

The study is published in the journal Nature Communications.

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<a href="/latest_stories/all/all/20" rel="author">Sumayah Aamir</a>
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