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Promising new research, has suggested a novel approach to Alzheimer's treatment.
Regular readers of this blog are familiar with the amyloid hypothesis which suggests that the most likely approach to treating or preventing Alzheimer's disease will be to somehow limit the accumulation of beta amyloid in the brain. Beta amyloid peptides are formed when a longer protein called amyloid precursor protein (APP) is chopped up into smaller fragments as part of the body's normal recycling process. This hypothesis is based on the fact that beta-amyloid is notably present in the form of a sticky plaque in all cases of Alzheimer's disease.
The new research, published in the Proceedings of the National Academy of Sciences, has determined that APP travels through the brain cells along a different pathway than the beta secretase enzymes that chop it up and aid the formation of the harmful plaques. This opens the opportunity for a "road block" strategy whereby it might be possible to limit the production beta-amyloid by preventing contact between APP and the enzymes that help to trasorm it into beta-amyloid. Doing so could possibly prevent unwanted side effects that sometimes arise from treatments that completely block or eliminate the production of otherwise important proteins and enzymes.
While this is science is promising, the implications are still uncertain and the new knowledge is only applicable at a very basic and hypothetical level. Nonetheless, it is another avenue through which scientists may soon be able to bring the amyloid hypothesis forward to a real world treatment against the rising threat of Alzheimer's disease.
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