Synapse may hold the key to potential new treatment for Alzheimer’s

A research team led by scientists from UNSW Australia has discovered how connections between the patient’s brain cells get destroyed during the initial stages of Alzheimer’s disease. This work provides scientists with fresh opportunity for carrying out research on potential cures for the degenerative brain disorder.

Dr. Vladimir Sytnyk, the study’s lead researcher, said that one of the very first signs that a person has developed Alzheimer’s disease is loss of synapses in his or her brain. For those who don’t know: synapses are structures in our brain that connect neurons. Dr. Sytnyk is a researcher representing the School of Biotechnology and Biomolecular Sciences at the UNSW.

Dr. Sytnyk added that synapses are needed for every single brain function, and more so for forming memories and learning. According to him, patients suffer loss of synapses during very early stages of Alzheimer’s disease, when they only experience mild cognitive impairment and much before their nerve cells start dying.

Dr. Sytnyk informed that he and his colleagues have discovered a new molecular mechanism that contributes to this loss of synapse directly. He feels that this discovery will eventually lead to development of new treatments for Alzheimer’s disease and allow early diagnosis of the condition.

During the study, researchers studied NCAM2 (neural cell adhesion molecule 2), a protein found in our brain. NCAM2 belongs to a family of molecules that is responsible for physically connecting membranes of our synapses and helping in stabilizing the enduring synaptic contacts between the neurons. The researchers used post-mortem brain tissues from individuals both with and without Alzheimer’s.

It was found that the levels of synaptic NCAM2 in the hippocampus of people with the degenerative brain disorder were lower compared to the ones without the condition.





Even mice studies and laboratory studies conducted by the researchers revealed that NCAM2 can be broken down by beta-amyloid, which is also a protein, and the primary component of plaques building up in brains of people suffering from Alzheimer’s disease.

According to Dr. Sytnyk, the researcher conducted by the team under him shows that there’s link between loss of synapses and loss of the protein NCAM2 and the toxic effects of beta-amyloid form the basis of that link.

Dr. Sytnyk believes this finding will allow scientists to carry out research to develop new treatments for preventing destruction of neural cell adhesion molecule 2 in our brain.