Much research has been done to understand Alzheimer's disease, but a new study conducted by researchers from the University of New South Wales (UNSW) in Australia shows a fascinating discovery of how brain cell connections are destroyed, taking research yet one step closer to finding a cure for the disease.
The researchers investigated post-mortem brain tissue from people with and without Alzheimer's disease. They found out that in people with Alzheimer's, synapses connecting brain cells called neurons are destroyed in the early stage of the disease, before the symptoms begin to appear.
"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," lead researcher Vladimir Sytnyk from the UNSW School of Biotechnology and Biomolecular Sciences said in a press release.
The membranes of these synapses are connected by a protein called neural cell adhesion molecule 2 (NCAM2). In the brain tissue of people with Alzheimer's, the researchers saw that the levels of NCAM2 were low, particularly in the hippocampus.
In studies involving mice, the researchers discovered that NCAM2 was destroyed by another protein called beta-amyloid, a major part of the plaque that builds up in the brain of Alzheimer's disease patients. "Our research shows the loss of synapses is linked to the loss of NCAM2 as a result of the toxic effects of beta-amyloid," Sytnyk said.
The discovery of this mechanism paves the way for the development of new treatments for Alzheimer's, the researcher 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," Sytnyk said. "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 online Nov. 27 in the journal Nature Communications.
