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Uncovering first molecular missteps that drive neurons in pathway leading to Alzheimer's disease
Date:12/15/2013

ather than by the plaques and tangles themselves," Dr. Bloom explained.

This new research to be presented at ASCB 2013 follows up on results published last spring when the UVA researchers described in greater detail how amyloid-beta activates multiple enzymes named protein kinases to add phosphates to specific sites on tau, setting neurons on the pathway to CCR.

Now in this new molecular "sequel," Dr. Bloom and lab members Andrs Norambuena and Lloyd McMahon implicate a novel group of proteins -- Rac1, Gαs (Gs alpha), and NCAM -- and two protein kinases complexes -- mTORC1 and mTORC2 -- as required participants to set off CCR.

Their identification reveals how a fundamental balance is upset, placing neurons on the road to AD. "The mTOR complexes are master regulators of cellular proliferation, growth and metabolism," Dr. Bloom said. "Most important, our results indicate that tau normally inhibits mTOR from promoting neuronal cell replication, but that this inhibition is reversed by an amyloid beta oligomer-induced, mTOR-dependent mechanism that modifies tau. In other words, tau and mTOR regulate each other."

This delicate balance is compromised by amyloid-beta oligomers in a way that allows neurons that should never replicate to re-enter the cell cycle. They fail to divide and eventually die instead. "Some of the earliest events in AD pathogenesis are therefore caused by amyloid-beta oligomers altering a fundamental neuronal signaling axis centered around tau and mTOR," proposed Dr. Bloom who said that he believes that the proteins identified in this signaling axis are potential biomarkers, and therapeutic targets for very early stages of AD, leaving the door open for an even more exciting sequel down the road.


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Contact: Cathy Yarbrough
cyarbrough@ascb.org
858-243-1814

John Fleischman
jfleischman@ascb.org

American Society for Cell Biology
Source:Eurekalert


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