Alzheimer's: a newly identified molecular mechanism opens new avenues

During the early stages of Alzheimer's disease, when individuals appear to be free of symptoms, toxic changes are nevertheless taking place in the brain - including synapse loss. Though scientists do not yet fully know what causes this form of dementia, researchers have now found how brain cell connections are destroyed in the early stages of the disease.

The researchers, led by scientists at the University of New South Wales (UNSW) in Australia, say their findings could lead to more research into possible treatments. They published their work the journal in Nature Communications.

Dr. Alois Alzheimer first identified Alzheimer's disease in 1906, after he observed changes in the brain tissue of a woman who had died of an odd mental illness, and had shown symptoms that included memory loss and unpredictable behavior.
Upon examining her brain after death, Dr. Alzheimer found abnormal clumps - now known as amyloid plaques - and tangled fibers - now called tau tangles.

The leader of this latest study, Dr. Vladimir Sytnyk, from the UNSW School of Biotechnology and Biomolecular Sciences, explains that loss of synapses - which connect brain neurons - is one of the first changes associated with Alzheimer's disease.
"Synapses are required for all brain functions," he says, "and particularly for learning and forming memories."
He adds that synapse loss occurs very early in Alzheimer's disease, long before the nerve cells die, when only mild cognitive impairment is noticeable.

Low NCAM2 levels found in brains affected by Alzheimer's

To further investigate brain changes related to Alzheimer's disease, Dr. Sytnyk and colleagues looked at a brain protein called neural cell adhesion molecule 2 (NCAM2), which is part of a family of molecules that connects synapse membranes, helping maintain synaptic connections between neurons.

By studying brain tissue from people with and without the condition who had died, the team found that synaptic levels of NCAM2 in the hippocampus were low in the individuals with the Alzheimer’s.
In Alzheimer's, most of the damage appears to take place in the hippocampus, which is the part of the brain that is essential in forming memories.

Furthermore, studies performed on mice revealed that NCAM2 was broken down by beta-amyloid proteins, which are the abnormal clumps that build up in the brains of people with Alzheimer's.

"We have identified a new molecular mechanism, which directly contributes to this synapse loss," says Dr. Sytnyk, "a discovery we hope could eventually lead to earlier diagnosis of the disease and new treatments."

Author: Marie Ellis
Text abridged and adapted / Nov.2015
With kind permission to publish from MNT
To read the complete article, please go to: Medical News Today

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