Authors: Alice Weatherston
Researchers from the University of New South Wales (Australia) have identified a novel molecular mechanism that may play a key role in the loss of synapses early in Alzheimer’s disease. The work, which was published recently in Nature Communications, highlights a potential new area of focus for the development of treatments for the degenerative disease.
The study focused on the protein termed neural cell adhesion molecule 2 (NCAM2), one of a range of molecules responsible for connecting the membranes of synapses and stabilizing neuronal synaptic contacts.
Utilizing post-mortem brain tissue from individuals with and without Alzheimer’s disease, the research team discovered that synaptic NCAM2 levels in the hippocampus were reduced in those with Alzheimer’s disease.
In addition, mouse studies indicated that NCAM2 was broken down by beta-amyloid, the protein basis of amyloid plaques characteristic of the brains of individuals with Alzheimer’s 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,” explained Vladimir Sytnyk (University of New South Wales), lead author of the study.
As well as highlighting possibilities for further treatment research into the prevention of NCAM2 destruction in the brain, the team believe that the discovery could help to improve diagnosis at an earlier stage of the disease. “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,” commented Sytnyk.