The synapse loss in the brain starts to take place during the onset of dementia, even when the patients show no external or recognizable symptoms at all. Although the reason behind the toxic damage to the brain is not understood completely, researchers at the University of New South Wales (UNSW) in Australia said that they have identified how brain cell connections are destroyed during the early stages of Alzheimer's.

The loss of synapses is linked to mild cognitive impairment in individuals with an early form of dementia. This process takes place long before the neurons actually start to die in such patients. Therefore, typical symptoms of the disease begin to appear at a later stage.

Researchers said that the identification of the molecular mechanism that leads to loss of synapse could pave the way for a treatment method that could potentially curb the progress of the disease at an early stage.

During the study, the UNSW researchers studied a protein called neural cell adhesion molecule 2 (NCAM2), derived from the brain tissue of people who had died with or without Alzheimer's disease. The research team decided to study NCAM2 because it is one of the molecules that helps maintain a connection between synapse and neurons and also keeps the membranes of the synapses together.

The team found that levels of synaptic NCAM2 in the hippocampus of people who had been diagnosed with Alzheimer's before their death was significantly lower. Hippocampus is the part of the brain that forms memory and emotions and where most damage occurs because of Alzheimer's.

In their study published in the journal Nature Communications, the researchers suggest that in such people, synaptic NCAM2 gets broken down by the beta-amyloid clumps that form in the brain of the Alzheimer's patients.

The research team is now planning to study NCAM2 loss as another potential option for treatment and diagnosis of the disease.

"Our research shows the loss of synapses is linked to the loss of NCAM2 as a result of the toxic effects of beta-amyloid,” said lead researcher Vladimir Sytnyk, in a press release. "It opens up a new avenue for research on possible treatments that can prevent the destruction of NCAM2 in the brain."