Beta-amyloid protein has long been implicated in the development Alzheimer's disease and is formed through the activity of several enzymes, including BACE1. While the enzyme has always been regarded of dangerous, new research has shown that its effects are more damaging than previously thought.
A study at Sanford-Burnham has found that BACE1 not only helps in the production of beta-amyloid proteins, but also regulates other cellular processes that lead to memory loss.
This has massive implications for treating Alzheimer's, as now instead of simply inhibiting the activity of the enzyme, it has to be eradicated altogether.
The discovery was made when Professor Huaxi Xu and his team used a mouse model that produced human BACE1 and analysed how it functioned independently of beta-amyloid production.
If the enzyme was only used to produce the toxic protein, the mice would experience no negative effects when this function was inhibited. However, impaired learning and memory was observed, indicating a secondary role was at work.
Understanding how the symptoms of Alzheimer's disease are brought about will prove key in developing key treatments for the condition and dementia.
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