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 themechanism by which connections in the brain are destroyed in theearly stages of Alzheimer's disease. The findings represent anotherangle of attack in the ongoing battle to find a cure for thewidespread degenerative condition.
Alzheimer's disease is a widespreadproblem, with an estimated 5.3 million people suffering from it in United States alone. A huge amount of effort is going into findingeffective 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 actualcure for the condition, gaining a full understanding of the processesit involves is key.
The UNSW-led study attacks the diseasefrom this angle, seeking to better understand how the conditionbreaks down the structures that connect neurons in the brain, knownas synapses. These connections are essential for all brain function,and especially for forming memories. It's known that they're brokendown early on by Alzheimer's, but exactly how this occurs was amystery.
The team focused on a protein known as neural cell adhesion molecule 2, or NCAM2 for short. Studyingpost-mortem brain tissue from the hippocampus – an area highly affected by the disease – the researchers discovered that NCAM2levels in synapses were lower in Alzheimer's sufferers than healthysubjects, suggesting that the protein plays a role in thedestruction.
Turning to laboratory mice, theresearchers were able to observe that the NCAM2 is actually broken down by a different protein called beta-amyloid. That name might wellring a bell with those familiar with the condition, as it's the maincomponent of the plaques that build up in the brain as the diseaseprogresses.
Overall, the study traces back thecause of the synapse loss to the effects of beta-amyloid. It's hopedthat this better understanding the process will allow for the futuredevelopment of more targeted preventative treatments.
The findings of the research were published in the journal Nature Communications.