Study shows how Alzheimer's disease destroys brain cell connections early on
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.
Alzheimer's disease is a widespread problem, with an estimated 5.3 million people suffering from it in United States alone. A huge amount of effort is going into finding effective treatments, and there have been a lot of positive results, with teams developing new drugs that tackle aspects of aging associated with the condition, and even using ultrasound therapy to combat plaque build-ups in the brain. In order to arrive at an actual cure for the condition, gaining a full understanding of the processes it involves is key.
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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.
The findings of the research were published in the journal Nature Communications.