Brain's efforts to save itself during Alzheimer's may backfire

The creation of a new transgenic mouse that makes a mysterious brain chemical may lead to better understanding of why people with Alzheimers disease lose their memory.

The neurotransmitter galanin appears to play a role in the disease, and scientists are now trying to figure out how and why. Galanin is normally neuro-protective, following brain injury. One possibility is that the brain overproduces galanin during the early stages of Alzheimers in an effort to rescue the afflicted brain but, over time, the brains own attempted cure makes a bad situation worse.

"This could be a sad irony. The body may be detecting the underlying pathology of Alzheimer's and tries to rescue deteriorating brain cells with increased expression of galanin. Very early on in the disease, galanin might even be having beneficial effects," said Dr. Robert Steiner, a professor in the departments of Obstetrics and Gynecology, and Physiology and Biophysics, at the University of Washington School of Medicine. "As the brain attempts to rescue itself with galanin and the disease progresses, the overexpression of galanin may become its own problem. This excess of galanin may contribute to the cognitive decline that Alzheimer's patients and their families so dread. "

The findings of Steiner and colleagues are published in the March 20 issue of Proceedings of the National Academy of Sciences. Co-authors include Dr. Jacqueline N. Crawley, chief of the Section on Behavioral Neuropharmacology, the National Institute of Mental Health; Dr. Elliott J. Mufson, professor in the Department of Neurological Sciences at Rush Presbyterian-St. Lukes Medical Center in Chicago; and Dr. John Hohmann, who was then a doctoral student in the neurobiology and behavior program at the University of Washington.

If galanin is playing a role in the disease, then what we know as Alzheimers could be the result of many parallel events that themselves create complications. Crawley said that galanin will need to b

Contact: Walter Neary
University of Washington

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