26 February 2019
Boston, MA, USA – Researchers have uncovered an enzyme and a biochemical pathway they believe may lead to the identification of drugs that could inhibit the production of beta-amyloid protein, the toxic initiator of Alzheimer’s disease (AD).
AD is characterized by the accumulation of beta-amyloid plaques, tau fibers and the loss of neurons in the brain. Currently, no FDA-approved drugs exist that attack the cause of disease.
After screening more than 75,000 small molecules, researchers at Boston University School of Medicine (BUSM) and Boston University discovered a molecule that reduced the formation of amyloid beta protein in cells grown in petri dishes.
“But more importantly we discovered the target of these molecules, an enzyme and a biochemical pathway that can be inhibited in Alzheimer’s to decrease amyloid production,” explained corresponding author Carmela Abraham, PhD, professor of biochemistry at BUSM.
According to the researchers, the inhibitors of this pathway are also anti-cancer therapies and are another example where cancer and neurodegeneration cross paths.
The researchers are optimistic that their study will open a new avenue of research to stall or even stop the buildup of beta-amyloid protein. “We are in desperate need of drugs that can treat or even prevent Alzheimer’s disease. Additional studies to improve our small molecules could lead to a disease-modifying pill for the millions who suffer from AD or those at high risk of developing the disease.”
These finding appear in the Journal of Alzheimer’s Disease.
NOTES FOR EDITORS
Full study: “Small Molecule Amyloid-β Protein Precursor Processing Modulators Lower Amyloid-β Peptide Levels via cKit Signaling” by CD Chen, E Zeldich, C Khodr, K Camara, TY Tung, EC Lauder, P Mullen, TJ Polanco, YY Liu, D Zeldich, W Xia, WE Van Nostrand, LE Brown, JA Porco Jr., and CR Abraham (DOI: 10.3233/JAD-180923) to be published in Journal of Alzheimer’s Disease, Volume 67, Issue 3 by IOS Press. The article is online at: content.iospress.com/articles/journal-of-alzheimers-disease/jad180923 .
Funding for this study was provided by grants from the Alzheimer’s Association, the Cure Alzheimer’s Fund and the Boston University Alzheimer’s Disease Center. Work at the BU-CMD is supported by R24-753 GM111625.
Gina DiVravio, Boston University (+1 617-358-7838; email@example.com).
About the Journal of Alzheimer's Disease
The Journal of Alzheimer's Disease (JAD) is an international multidisciplinary journal to facilitate progress in understanding the etiology, pathogenesis, epidemiology, genetics, behavior, treatment and psychology of Alzheimer's disease. The journal publishes research reports, reviews, short communications, book reviews, and letters-to-the-editor. Groundbreaking research that has appeared in the journal includes novel therapeutic targets, mechanisms of disease and clinical trial outcomes. JAD has an Impact Factor of 3.476 according to the 2017 Journal Citation Reports (Clarivate Analytics, 2018). j-alz.com
About IOS Press
IOS Press is headquartered in Amsterdam with satellite offices in the USA, Germany, India and China and serves the information needs of scientific and medical communities worldwide. IOS Press now publishes over 100 international journals and about 75 book titles each year on subjects ranging from computer sciences and mathematics to medicine and the natural sciences. iospress.com