Over 100 years have passed since Alzheimer’s disease was discovered, yet the mechanisms behind the disease have remained poorly understood.
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