Gladstone/UCSF team discovers interaction of two brain proteins may be key factor in development of Alzheimer's disease

tists have failed to find such a relationship. The Gladstone and UCSF researchers found that high levels of A-beta can be neurotoxic even without plaque formation. Mucke noted, "These results could provide a circuit-level explanation for the discrepancies observed between plaque load and functional deficits in people with AD."

In this earlier study, Mucke and his collaborators used genetic engineering to produce transgenic mice with mutant human APP and A-beta in the brain. Their findings showed that high levels of A-beta disrupted the structure and function of nerve cell circuits in the hippocampus, a brain region that is essential for the formation of memories. In addition, they found that amyloid proteins induced degeneration of synaptic connections and impeded the ability of neurons to transmit nerve impulses. These abnormalities increased with age, similar to the pattern in AD.

"Remarkably, the amyloid-induced disruption of memory circuits was found in the transgenic mice even before they developed AD-like amyloid plaques. This demonstrates that plaque formation is not required for amyloid peptides to impair the communications between nerve cells in the brain," said Nicoll, who directed the electrophysiological analysis of the mice.

According to Mucke, the findings have important implications for the design of new treatments for AD. "Inhibiting plaque formation alone may not be enough to prevent A-beta toxicity in the brain. Inhibition of A-beta production may be required to achieve this therapeutic goal," he said.

In addition to Mucke and Xu, co-investigators of the June 22 PNAS paper are Daseng Yang, PhD; Tony Wyss-Coray, PhD; Jim Yan, BS; and Li Gan, PhD, all from the Gladstone Institute of Neurological Disease and UCSF Department of Neurology, and Yi Sun, MD, PhD, of Parke-Davis Pharmaceutical Research. This research was supported by grants from the National Institute on Aging and from the Alzheimer's Disease Program of the State of

Contact: Corinna Kaarlela
University of California - San Francisco

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