New research has discovered how connections between brain cells are destroyed in the early stages of Alzheimer’s disease, which could open up a new avenue for research on possible treatments for the degenerative brain condition.
“One of the first signs of Alzheimer’s disease is the loss of synapses — the structures that connect neurons in the brain,” said Dr. Vladimir Sytnyk, of the University of New South Wales School of Biotechnology and Biomolecular Sciences in Australia, and lead author of the study.
“Synapses are required for all brain functions, and particularly for learning and forming memories,” he continued. “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.”
The researchers identified a new molecular mechanism that directly contributes to this synapse loss, he said.
For their research, the researchers studied a protein in the brain called neural cell adhesion molecule 2 (NCAM2), one of a family of molecules that physically connects the membranes of synapses and help stabilize these long-lasting synaptic contacts between neurons.
Using post-mortem brain tissue from people with and without Alzheimer’s, they discovered that synaptic NCAM2 levels in the part of the brain known as the hippocampus were low in those with Alzheimer’s disease.
The researchers also showed in mice studies and in the laboratory that NCAM2 was broken down by another protein called beta-amyloid, which is the main component of the plaques that build up in the brains of people with 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 Sytnyk. “It opens up a new avenue for research on possible treatments that can prevent the destruction of NCAM2 in the brain.”
The study was published in the journal Nature Communications.
Source: University of New South Wales