Alzheimer’s disease is the sixth leading cause of death in the U.S., annually killing more than 120,000 people. There is no treatment that can effectively prevent or slow this disease. An estimated 5.8 million Americans age 65 or older have Alzheimer’s, and that number is expected to more than double over the next 30 years.

The characteristic of the disease is the slowly progressive destruction of nerve cells and nerve cell contacts. One of the characteristic morphological features is the accumulation of the peptide amyloid-ß in the brain in the form of plaques and vascular amyloids.  In spite of numerous researches, also with animal "models
there is no cure yet.

It is already known that the blood-brain barrier ABC transporter ABCC1, a membrane protein that actively transports substances across the membrane, exports amyloid-ß from the endothelial cells of the blood-brain barrier to the periphery, and that pharmaceutical activation of ABCC1 can reduce the deposition of amyloid plaques in the brain.

Scientists from the Translational Genomics Research Institute (TGen), led by Matt Huentelman, Ph.D. and TGen professor of neurogenomics, have now shown that ABCC1 not only shuttles amyloid-ß out of cells, but also modifies the amyloid precursor protein (APP) production. In addition, they were able to observe that the drug thiethylperazine, which has long been used to relieve nausea and vomiting, increases ABCC1 transport activity.

This could provide a new target for the treatment of Alzheimer's disease.

Original paper:
Wayne M. Jepsen et al (2021). Adenosine triphosphate binding cassette subfamily C member 1 (ABCC1) overexpression reduces APP processing and increases alpha- versus beta-secretase activity, in vitro. Biology Open.

Source:
https://www.tgen.org/news/2021/april/13/tgen-identifies-gene-for-alzheimers-treatment/