Washington, Sep 6 (IANS) Scientists have discovered that eliminating an enzyme from mice with Alzheimer's symptoms virtually eliminates a compound behind the development of plaques.
The compound is 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, symptomatic of Alzheimer's.
"These mice are models for the most aggressive form of Alzheimer's disease and produce the highest amount of A-beta peptides," Sung Ok Yoon, associate professor of molecular and cellular biochemistry at Ohio State University, who led the study, was quoted as saying by the journal Neuron.
"This 90 percent reduction is the biggest drop in A-beta levels that has been reported so far by treating animal models with drugs or genetic manipulations," added the researcher, according to a university statement.
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. Alzheimer's disease affects more than five million Americans, and its cause remains unknown.
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