A research team led by scientists from the University of New South Wales (UNSW) in Australia has studied the mechanism by which connections in the brain are destroyed in the early stages of Alzheimer's disease. The findings represent another angle of attack in the ongoing battle to find a cure for the widespread degenerative condition.
The UNSW-led study attacks the disease from this angle, seeking to better understand how the condition breaks down the structures that connect neurons in the brain, known as synapses. These connections are essential for all brain function, and especially for forming memories. It's known that they're broken down early on by Alzheimer's, but exactly how this occurs was a mystery.
The team focused on a protein known as neural cell adhesion molecule 2, or NCAM2 for short. Studying post-mortem brain tissue from the hippocampus – an area highly affected by the disease – the researchers discovered that NCAM2 levels in synapses were lower in Alzheimer's sufferers than healthy subjects, suggesting that the protein plays a role in the destruction.
Turning to laboratory mice, the researchers were able to observe that the NCAM2 is actually broken down by a different protein called beta-amyloid. That name might well ring a bell with those familiar with the condition, as it's the main component of the plaques that build up in the brain as the disease progresses.
Overall, the study traces back the cause of the synapse loss to the effects of beta-amyloid. It's hoped that this better understanding the process will allow for the future development of more targeted preventative treatments.
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