Public Release:  Promising compound restores memory loss and reverses symptoms of Alzheimer's

New research in the FASEB Journal by NIH scientists suggests that a small molecule called TFP5 rescues plaques and tangles by blocking an overactive brain signal, thereby restoring memory in mice with Alzheimer's

Federation of American Societies for Experimental Biology

A new ray of hope has broken through the clouded outcomes associated with Alzheimer's disease. A new research report published in January 2013 print issue of the FASEB Journal by scientists from the National Institutes of Health shows that when a molecule called TFP5 is injected into mice with disease that is the equivalent of human Alzheimer's, symptoms are reversed and memory is restored--without obvious toxic side effects.

"We hope that clinical trial studies in AD patients should yield an extended and a better quality of life as observed in mice upon TFP5 treatment," said Harish C. Pant, Ph.D., a senior researcher involved in the work from the Laboratory of Neurochemistry at the National Institute of Neurological Disorders at Stroke at the National Institutes of Health in Bethesda, MD. "Therefore, we suggest that TFP5 should be an effective therapeutic compound."

To make this discovery, Pant and colleagues used mice with a disease considered the equivalent of Alzheimer's. One set of these mice were injected with the small molecule TFP5, while the other was injected with saline as placebo. The mice, after a series of intraperitoneal injections of TFP5, displayed a substantial reduction in the various disease symptoms along with restoration of memory loss. In addition, the mice receiving TFP5 injections experienced no weight loss, neurological stress (anxiety) or signs of toxicity. The disease in the placebo mice, however, progressed normally as expected. TFP5 was derived from the regulator of a key brain enzyme, called Cdk5. The over activation of Cdk5 is implicated in the formation of plaques and tangles, the major hallmark of Alzheimer's disease.

"The next step is to find out if this molecule can have the same effects in people, and if not, to find out which molecule will," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal. "Now that we know that we can target the basic molecular defects in Alzheimer's disease, we can hope for treatments far better - and more specific - than anything we have today."

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Receive monthly highlights from the FASEB Journal by e-mail. Sign up at http://www.faseb.org/fjupdate.aspx. The FASEB Journal is published by the Federation of the American Societies for Experimental Biology (FASEB). It is among the most cited biology journals worldwide according to the Institute for Scientific Information and has been recognized by the Special Libraries Association as one of the top 100 most influential biomedical journals of the past century. FASEB is composed of 26 societies with more than 100,000 members, making it the largest coalition of biomedical research associations in the United States. Celebrating 100 Years of Advancing the Life Sciences in 2012, FASEB is rededicating its efforts to advance health and well-being by promoting progress and education in biological and biomedical sciences through service to our member societies and collaborative advocacy.

Varsha Shukla, Ya-Li Zheng, Santosh K. Mishra, Niranjana D. Amin, Joseph Steiner, Philip Grant, Sashi Kesavapany, and Harish C. Pant. A truncated peptide from p35, a Cdk5 activator, prevents Alzheimer's disease phenotypes in model mice. FASEB J. January 2013 27:174-186; doi:10.1096/fj.12-217497; http://www.fasebj.org/content/27/1/174.abstract

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