Scientists have found that eliminating an enzyme from mice with symptoms of Alzheimer’s disease leads to a 90 percent reduction in the compounds responsible for formation of the plaques linked to Alzheimer’s disease. That's the biggest drop in A-beta levels that has been reported so far by treating animal models with drugs or genetic manipulation. The compounds are amyloid beta, or A-beta peptides; peptides are proteins, but are shorter in length. When A-beta peptides accumulate in excessive amounts in the brain, they can form plaques, which are a hallmark of Alzheimer’s disease. The key to reducing A-beta peptides was the elimination of an enzyme called jnk3. This enzyme stimulates a protein that produces A-beta peptides, suggesting that when jnk3 activities are high, A-beta peptide production increases – increasing chances for their accumulation and formation into plaques.
The researchers also observed that jnk3 activities in brain tissue from Alzheimer’s disease patients were increased by 30 to 40 percent when compared to normal human brain tissue. Jnk3 activity typically remains low in the brain, but increases when physiological abnormalities arise. The findings suggest that jnk3 could be a new target for Alzheimer’s disease intervention, Yoon said. So far, some drugs can slow the disease’s progression, but there is no cure.
Alzheimer’s disease affects more than 5 million Americans, and its cause remains unknown. Although scientists have not yet determined whether A-beta peptides present in plaques cause Alzheimer’s disease or form as a consequence of the disease, the presence of the plaques is linked to progressive cognitive decline.
Via Dr. Stefan Gruenwald