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Scientists zero in on memory-related proteins at the core of Alzheimer's disease

New research sheds light on how the formation of long-term memories may be blocked in Alzheimer's disease.

Reporting in two companion papers in the October 19 issue of the Journal of Neuroscience, investigators from the Gladstone Institute of Neurological Disease show in genetically engineered mouse models of the disease that the accumulation of Alzheimer-related neurotoxic amyloid-beta (Aβ) peptides can deplete key proteins in a specific memory center of the brain. They also report that this process can be worsened by increased activity of an enzyme called Fyn.

The inability of Alzheimer's patients to remember events from a few days ago may be linked to the lack of proteins that strengthen the contact points, or synapses, between neurons in the brain, according to study findings.

Much research points to the idea that, far from having a single cause, Alzheimer's disease is typically brought on by a combination of risk factors. In keeping with that model, these papers show that the depletion of memory proteins can require the interaction of different disease-promoting molecules, explains GIND Director Lennart Mucke, MD, the Joseph B. Martin Distinguished Professor in Neuroscience at the University of California, San Francisco, and senior author of the papers.

The researchers found that memory proteins can be depleted not only by high levels of Aβ but also by low levels of Aβ in combination with high levels of Fyn activity.

"Like partners in crime, Aβ and Fyn appear to cooperate to cause Alzheimer-like changes in the brain," says Mucke. The findings may eventually help identify novel therapeutic targets and biomarkers for emerging treatments.

Scientists in Mucke's laboratory were among the first to generate genetically engineered mice that produce human Aβ, providing a powerful tool to study the devastating disease. Using a technique called gene expression imaging to profile mole
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Contact: John Watson
jwatson@gladstone.ucsf.edu
415-734-2019
Gladstone Institutes
18-Oct-2005


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