Alzheimer's Disease Cure 2017 News: Scientists Discover How Disease Starts, Finds a Solution From There
Scientists may have found a way to slow down or ultimately prevent Alzheimer's disease. The key is to understand how the disorder starts.
The researchers at the University of North Carolina (UNC) at Chapel Hill found that this involves the immune cells and two deposits of protein — amyloid beta and tau.
It turns out that the amyloid beta — specifically oligomers, which are believed to be the most harmful form of it — sets off the immune cells resulting in inflammation that "floods" the neurons with calcium and harms them.
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This, in turn, creates "bead-like swellings" or "neuritic beads" filled with abnormal tau. Two other proteins, namely MMP-9 and HDAC6 also appear to advance the formation of these beads.
Research head Todd Cohen, Ph.D., an assistant professor of neurology at UNC, revealed in a journal on Cell Reports that finding a way to stop these bead formations could help the neurons become more resistant to Alzheimer's disease.
This probably leads to a snowball effect. Tau detaches from microtubules and is trafficked throughout the neuron, ending up in these beads. One possibility is that these tau-filled beads are the sites where the classic tangle-like aggregates of tau will eventually emerge, which is the hallmark of Alzheimer's disease.
However, it is the MMP-9 and HDAC6 that accelerates the build-up of these neuritic beads. When Cohen's group blocked the latter, the beads stopped forming.
This leads them to believe that HDAC6 inhibitors could work with drug developers already testing them. What is yet to be made clear is how they work. Cohen and company also believe that these inhibitors "inform the development of other kinds of inhibitors that affect this cascade, particularly those that might impact cognitive processes."
Blocking HDAC6 and MMP-9 could also help with regard to other neurodegenerative diseases that feature neuritic beading such as head injuries in healthy brains, which Cohen speculates that bead formations could be early signs of cognitive decline.
The researchers aim to continue to study the process involving the amyloid beta and tau as they crack the code for a cure:
If we can demonstrate this cascade in a wild-type mouse, then we'll be able to study Alzheimer's and test therapies in ordinary lab mice without the need for artificial genetic engineering used in traditional Alzheimer's mouse models.
