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Scientists demonstrate means of reducing Alzheimer's-like plaques in fly brain
Date:7/15/2008

Thomas Jefferson University in Philadelphia, sought to turn the tables. If NEP deficiency caused pathology, what would happen if NEP enzymes were expressed in above-normal amounts in brain cells affected by beta amyloid plaques?

Using transgenic fruit flies, the team found that by overexpressing human NEP in fly neurons, accumulation of Aβ42 inside the neurons was reduced. The scientists also observed that outright death of neurons due to Aβ42 plaques was suppressed.

At the same time, the experiment produced results that were not at all encouraging. Although NEP overexpression fought off plaques, chronic overexpression in the fly brain caused age-related degeneration of the axons that connect nerve cells, and also shortened the lifespan of the flies. The team believes that this effect was caused by the unintended impact of chronic NEP activity upon a critical gene-regulating protein, a transcription factor called CREB.

The team wants to test whether the life-shortening impact of NEP overexpression upon CREB occurs in transgenic mammals -- for instance, in mice, which are genetically closer to humans than flies.

"We have succeeded in demonstrating both protective and detrimental aspects of high NEP activity in the fly brain," Dr. Zhong said. "We also noted a reduction of NEP activity in fly brains that correlates with age. These are intriguing clues about mechanisms that contribute to the causation of Alzheimer's.

"We must now seek additional knowledge about the physiological mechanisms that underlie age-dependent downregulation of NEP in flies. This is a powerful genetic model system that we hope will lead us to discover novel therapeutics to combat Alzheimer's, a disease that devastates so many people every year."


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Contact: Jim Bono
bono@cshl.edu
516-367-8455
Cold Spring Harbor Laboratory
Source:Eurekalert

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