Scientists at the University of New South Wales have identified how connections between brain cells are destroyed in the early stages of Alzheimer’s disease. Their findings were published on November 27 in the journal Nature Communications.
Over 100 years have passed since Alzheimer’s disease was discovered, yet the mechanisms behind the disease have remained poorly understood.
Alzheimer’s disease is a progressive disease that destroys memory and causes cognitive decline. One of the key signs of early Alzheimer’s is the loss of synapses, structures that connect neurons in the brain. Synapses allow information to flow between neurons. They are required for all brain functions, particularly for learning and forming memories. Loss of synapses occur before clinical symptoms of Alzheimer’s are apparent and long before the nerve cells themselves die.
Molecular biologist Vladimir Sytnyk led a team of researchers to investigate brain changes related to Alzheimer’s. They focused on a protein in the brain called neural cell adhesion molecule 2 (NCAM2). NCAM2 is important for brain development and necessary in adult brains. Previous studies have indicated a link between NCAM2 and Alzheimer’s disease. The team now wanted to know whether the disease influenced levels of NCAM2 in synapses.
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The team studied frozen post-mortem hippocampus brain tissue of Alzheimer’s disease patients and non-affected controls. They found that NCAM2 levels in synapses were lower in Alzheimer’s suffers than in healthy patients.
The team additionally used mice to find whether a different protein, beta-amyloid, interacted with NCAM2 in the brain. Beta-amyloid is the main component of the amyloid plaques found in the brains of Alzheimer patients. These plaques accumulate outside neurons and destroy them. The scientists observed that beta-amyloid broke down NCAM2.
Overall, the data provides a mechanical explanation for the NCAM2 changes in synapses in Alzheimer’s disease brains: beta-amyloid causes synaptic loss and the breakdown of protein NCAM2.
The researchers hope the finding will allow for the future development of more targeted preventative treatments. "It opens up a new avenue for research on possible treatments that can prevent the destruction of NCAM2 in the brain," Sytnyk said.
Source:
Journal article and
University of New South Wales press release via
EurekAlert
