Researchers from UNSW have identified the mechanism by which connects between brain cells are destroyed in early stages of Alzheimer's disease
Researchers from University of New South Wales have found how communication between brain cells destroys in the early stage of Alzheimer’s disease. Every brain cell talks to its nearby cells and sends and receives signals through connections called synapses. But as we grew older, the process starts to deteriorate and result in synaptic loss. And scientists have identified the mechanism which directly contributes to this synapse loss.
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Alzheimer’s is a progressive disorder that negatively affects brain nerve cells and result in memory loss and disruption in thinking ability. An estimated 5.3 million people suffer the disease in U.S. alone. This discovery can help diagnose Alzheimer’s much earlier and may lead to new improved treatments for the disease.
“One of the first signs of the disease is the loss of synapses – the structures that connect neuron in the brain,” said lead author Dr Vladimir Sytnyk. “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.”
Researchers have studied thoroughly a protein in the brain called neural cell adhesion molecule 2, or NCAM2. The protein physically connects the membranes of synapses and helps them stabilize.
Researchers have found synaptic NCAM2 levels in the part of brain known as hippocampus were low in those who were diagnosed with disease compared to those who were not. Another protein called beta-amyloid destroys NCAM2. Beta-amyloid is toxic for nerve cells and develops a plague in Alzheimer’s brain.
“Our research shows that the loss of synapses is linked to the loss of NCAM2 as a result of the toxic effects of beta-amyloid,” said Dr Sytnyk.
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“It opens up a new avenue for research on possible treatments that can prevent the destruction of NCAM2 in the brain.”