BACE1: Target For A Potential Alzheimer’s Disease Cure

Alzheimer’s disease (AD) is one of the most common forms of dementia that causes memory and behavioral problems. It is a progressive disease with most cases starting in people over 65 years old. Initially, the symptoms are often attributed to ageing or stress. During the advanced stages, patients are completely dependent on caregivers, making AD one of the most costly diseases to manage. Currently, there are no treatments to stop or reverse disease progression. However, some treatments can improve the quality of life and slow the worsening dementia symptoms. There are many hypotheses for the cause of Alzheimer’s including genetics, amyloid plaques and tau protein abnormalities. Presently, there are no effective measures in preventing AD, although a healthy diet and lifestyle may reduce the risk of developing Alzheimer’s.

A recent report examined the effects of a drug called Verubecestat in AD human and animal trials. The drug targets the production of protein plaques that are associated with AD. The drug functions as a BACE1 (beta-site amyloid precursor protein cleaving enzyme 1) inhibitor involved in producing a protein called amyloid beta that forms the plaques. Amyloid is formed when amyloid precursor protein (APP) is cleaved by BACE1 and gamma-secretase. Plaque buildup in the brain may lead to neurodegeneration therefore, by blocking BACE1, the build-up of amyloid beta could be avoided to slow down or prevent AD development. The BACE1 inhibitor is now progressing to phase 3 clinical trials involving 1,500 patients before it can be given to AD patients. Promisingly, no major side effects have been identified.

For more information: http://stm.sciencemag.org/content/8/363/363ra150.full

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