Enzyme linked to plaque formation in Alzheimer's discovered

Washington: Scientists have found that eliminating an enzyme in Alzheimer's patients can lead to a 90 percent reduction in the compounds responsible for formation of plaques in the brain.

When A-beta peptides accumulate in excessive amounts in the brain, they can form plaques, which are a hallmark of Alzheimer's disease.

Researchers from the Ohio State University found that the key to reducing A-beta peptides in laboratory mice studies 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.

Pic used for representational purposes only.

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," lead author of the study, Sung Ok Yoon, said.

Researchers deleted jnk3 genetically from Alzheimer's disease model mice carrying the mutations that are found among early-onset Alzheimer's disease patients.

In six months, the deletion of the enzyme had lowered A-beta peptide production by 90 percent, which persisted over time, with a 70 percent reduction seen at 12 months in these mice.

The deletion of jnk3 improved cognitive function significantly, reaching 80 per cent of normal, while cognitive function in disease model mice was 40 per cent of normal.

The number of brain cells, or neurons, in the Alzheimer's disease mice was also increased with jnk3 deletion, reaching 86 percent of the value in normal mice, while the neuron

numbers were only 74 percent in Alzheimer's model mice. The research was published in the journal Neuron.


Updated Date: Sep 06, 2012 17:03 PM

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