Sydney, Australia – Researchers at the University of New South Wales (UNSW) found the reason why Alzheimer’s disease breaks the link between neurons. The study was published in the journal Nature Communications, and scientists say their findings could be an important clue for further research on new treatments.
Dr. Vladimir Sytnyk, lead researcher from UNSW’s School of Biotechnology and Biomolecular Sciences, explained how neuronal links are destroyed during the first stages of the disease.
“One of the first signs of Alzheimer’s disease is the loss of synapses — the structures that connect neurons in the brain. 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,” he reported.
This process occurs despite the fact that patients regularly seem asymptomatic during the early stages of Alzheimer’s when their brains start to lose many neurons as synapses are severed.
The researchers ultimately found a molecular mechanism that, according to Sytnyk, directly contributed to synapse loss: a brain protein by the name of neural cell adhesion molecule 2 (NCAM2), which belongs to a molecule family responsible for connecting the membranes of synapses and stabilizing neuronal links.
Scientists studied post-mortem brain tissue from Alzheimer’s patients and contrasted it with post-mortem brain tissue from non-sufferers. They concluded that patient’s NCAM2 levels in the hippocampus, which is one of the first areas of the brain targeted by Alzheimer’s, were low compared to those of people without the disease.
Sytnyk believes that knowing the synapses loss process in the hippocampus could lead to an early diagnosis of the disease and also help scientists develop new, more effective treatments for Alzheimer’s.
There is more to the research, though. After experimenting on mice, scientists additionally discovered that NCAM2 is actually severed by another brain protein called beta-amyloid, which can be found in the plaque-like formation covering the brains of people who suffer from Alzheimer’s.
Further understanding of the inner workings of the disease is crucial for the investigation of therapies and possibly a cure to Alzheimer’s.
Source: The Monitor Daily