ScienceDaily (Nov. 25, 2009) — Alzheimer's disease is thought to be caused by the build-up of a brain peptide called amyloid-beta. That's why eliminating the protein has been the focus of almost all drug research pursuing a cure for the devastating neurodegenerative condition.
A model of the human brain. New research suggests that amyloid-beta peptide -- the buildup of which in the brain is believed to cause Alzheimer's disease -- is also necessary to maintain proper brain functioning. (Credit: iStockphoto/Mark Evans
But that may be counterproductive, says Dr. Inna Slutsky of Tel Aviv University's Department of Physiology and Pharmacology, Sackler Faculty of Medicine. Her recent research demonstrates that amyloid-beta is also necessary to maintain proper brain functioning.
These findings may shake the foundations of Alzheimer's research.
In a new study published this month in Nature Neuroscience, Dr. Slutsky finds that amyloid-beta is essential for normal day-to-day information transfer through nerve cell networks in the brain. "If this protein is removed from the brain," says Dr. Slutsky, "as some drugs in development attempt to do, it may cause an impairment of neuronal function, as well as a further and faster accumulation of amyloid-beta in Alzheimer's."
A reset button for drug researchers
Without amyloid-beta, a normal product of cellular metabolism, one's ability to learn and remember could be profoundly damaged, so drugs currently in development to eliminate amyloid-beta could be rendered obsolete. With Dr. Slutsky's research, a leap in understanding the cause and development of Alzheimer's disease, however, new, more effective drug therapies could be developed.
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Journal Reference:
Efrat Abramov, Iftach Dolev, Hilla Fogel, Giuseppe D Ciccotosto, Eyal Ruff & Inna Slutsky. Amyloid-β as a positive endogenous regulator of release probability at hippocampal synapses. Nature Neuroscience, 2009; DOI: 10.1038/nn.2433
