Alzheimer's Disease: A Smoking Gun With No Suspect

By Bioradiations Staff

For the past three decades, beta-amyloid has been the assumed culprit of Alzheimer’s disease (AD). Consequently, a significant amount of research and industry resources have been deployed to understanding how it causes the disease, which has reached epidemic proportions (Alzheimer’s Association).

Beta-amyloid is a protein fragment that builds up in the brains of AD patients creating sticky clumps of plaque that disrupt communication between brain cells and eventually kills them.

The association between a patient with dementia and the buildup of amyloid plaques in the brain was first described by Dr. Alois Alzheimer in 1906. However, it wasn’t until 1984 that beta-amyloid was considered a diagnostic marker and target for AD treatment due to the work of Dr. George Glenner at University of California San Diego. Dr. Glenner created a brain bank to study the diseased brains of patients who were suspected to have died from AD. After discovering beta-amyloid deposits in over 90% of diseased brains, he characterized the protein as “a novel cerebrovascular amyloid protein,” responsible for the brain plaques in AD and a prime suspect in triggering nerve cell damage.

Based on Dr. Glenner’s findings, beta-amyloid became a natural focus of research on AD. Since then, the number of publications on this biomarker has skyrocketed.