Soluble amyloid precursor proteins can interact with specialized enzymes to reduce the accumulation of other, more harmful amyloid proteins reports a paper in Nature Communications this week. The study provides new insight into a unique balancing act that can often fail, contributing to the development of Alzheimer's disease. Amyloid precursor protein processing can sometimes go awry, leading to over-production of disease causing amyloid peptides. Accumulation of these peptides leads to the plaques that are commonly associated with Alzheimer's disease. A soluble amyloid precursor protein species known as sAPP-alpha acts against this process, preventing the onset of Alzheimer's disease.
Jun Tan and colleagues investigate the effects of administering sAPP-alpha to Chinese hamster ovary cells that are engineered to express disease causing amyloid proteins. They find that it reduces the amount of harmful amyloid proteins that are produced within the hamsters. They then go on to genetically manipulate transgenic mice with Alzheimer's disease-like pathology so that they also overexpressed sAPP-alpha They find that overexpressing sAPP-alpha decreases the level of amyloid plaques by interfering with the activity of a special secretase enzyme known as BACE1.
The authors suggest that the development of drugs which interfere with BACE1 activity as well as drugs which mimic sAPP-alpha could be beneficial in treating Alzheimer's disease
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