The findings of the study were detailed in the Journal of Experimental Medicine by the team from the Cleveland Clinic Lerner Research Institute in the U.S.. The authors achieved these results by gradually depleting an enzyme that plays a part in the formation of the plaques, known as BACE1.
But, how is Alzheimer's in a patient identified? This is done through an abnormal buildup of beta-amyloid peptide, a protein that can build into the large amyloid plaques in the brain that are a telltale sign of the deadly, and incurable disease. BACE1 helps produce beta-amyloid peptide. For this reason, inhibiting the enzyme with drugs could ultimately open the door to effective Alzheimer's treatments by halting the buildup.
Furthermore, researchers also tested the hypothesis by engineering a group of mice that lose the BACE1 enzyme as they grow older. While mice that lacked the enzyme altogether were found to suffer neurological defects, those who stopped producing it over time remained healthy. In order to discover how this new genetic makeup performs against Alzheimer's the researchers then bred their healthy mice with others engineered to develop the disease. In doing so, they found that while amyloid plaques started building up in the brain of the offspring, they also disappeared as the mice progressively lost the BACE1 enzyme.
The authors explained that such promising result don't come without caveats. Firstly, the experiment has only been performed in a mouse model, and as you can imagine there is no guarantee that comparable results will be achieved in humans. In addition, BACE1 takes part in many other important processes in the body, and drugs that progressively destroy it could have serious side effects.
Unfortunately, treating Alzheimer's disease is a difficult and often heartbreaking process. The research discovered here is neither a miracle nor is it a missed target. It might be the first step towards realizing such an effective treatment. Given these early results, it seems to be a worthwhile avenue to pursue.