NCAM2 and beta-amyloids are involved in Alzheimer’s progression.
Scientists from the University of Australia are now able to offer patients that suffer from Alzheimer’s disease, a new ray of hope. The team of researchers has managed to explain why Alzheimer’s breaks down links between neurons.
In the early stages of Alzheimer’s, patients are usually asymptomatic. Although this is a proven fact, the team states that even in the earliest stages of the disease, the brain loses a lot of neurons, because the disease is capable of severing the link between neurons.
By taking a look at the actual process, the team was capable of ascertaining how we actually lose synaptic coherence during the early stages of Alzheimer’s. A neuroscientist, by the name of Sytnyk, explains that the process of synaptic destruction occurs in the first stages of the disease, commonly regarded as mild cognitive impairment.
They were actually able to identify and isolate an entire molecular process, which ultimately led to plaque-like formation. This process is consistent with the final stages of Alzheimer’s. NCAM2, or neural cell adhesion molecule 2, is the name of the molecular compound which plays a significant role in the process of neuron communication. According to the scientists NCAM2’s is capable of actually stabilizing and strengthening the synaptic link between several neurons.
So, what is the connection between NCAM2 and the final stages of Alzheimer’s? The team explained that during the early onset of the disease, NCAM2 levels in the hippocampus, one of the first areas targeted by Alzheimer’s, are very low, compared to the NCAM2 levels of a healthy, non-affected person.
By researching how the protein loses coherence inside the hippocampus, the team could develop more targeted therapies for Alzheimer’s. Moreover, by understanding the inner working of the disease, they will be capable of diagnosing someone with Alzheimer’s much earlier.
To add some depth to the project, there is another fact which we must take into consideration. It would seem that the NCAM2 levels don’t go down on their own. There is another factor missing which could very well complete the puzzle.
Extensive laboratory research performed on mice has revealed the NCAM2 protein is broken down by another protein residing in the brain. Beta-amyloids have been discovered to play a lead role in NCAM2’s demise. Beta-amyloid is the protein usually found in the plaque-like formation that covers the brains of the people affected by Alzheimer’s.
The discovery of this molecular process can be construed as being a huge discovery for the medical sciences, because it can very well lead to new therapies, new medication and, why not, a cure in the nearby future.
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