Neuroscientists discover early signs of Alzheimer's Disease at synaptic level

Neuroscientists discover early signs of Alzheimer's Disease at synaptic level

At an early stage of Alzheimer’s disease, researchers from the University of New South Wales have found important information about how the connections between brain cells suffer. The research team led by Dr Vladimir Sytnyk, of the UNSW School of Biotechnology and Biomolecular Sciences has found important link between the early stage neural connections and the decline in cognitive abilities. Synapses are important for all brain functions but their role is even more important in case of forming memories and learning abilities among humans.

The research team has found the molecular mechanism that has direct link to synapse loss. The research could help in improving the treatment options for Alzheimer’s patients or individuals at risk of developing the condition at a later stage.

The research team analyzed in detail a protein in the brain called neural cell adhesion molecule 2, or NCAM2 - one of a family of molecules that physically connects the membranes of synapses and help stabilize these long lasting synaptic contacts between neurons. The research has been published in the latest issue of the journal Nature Communications.

Commenting about the research project, Dr. Sytnyk said, “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.”

Alzheimer’s disease impacts more than 30 million people across the world, according to the data collected for year 2012. For most patients, Alzheimer’s disease started over age of 65. No treatments stop or reverse its progression, though some may temporarily improve symptoms. In developed countries, AD is one of the most financially costly diseases.

Neuroscientist Dr Vladimir Sytnyk, who led the research at the University of New South Wales in Australia said the discovery could lead to considerably more effective treatment of a condition which still has no cure.

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 disease.

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.

Additionally, through mice studies, the researchers found 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.

The genetic heritability of Alzheimer's disease (and memory components thereof), based on reviews of twin and family studies, range from 49% to 79%. Around 0.1% of the cases are familial forms of autosomal (not sex-linked) dominant inheritance, which have an onset before age 65.

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