[ExI] [tt] Promising compound restores memory loss and reverses symptoms of Alzheimer's (in mice) (fwd)

[Tomasz Rola]

(Of course, mice are not humans and vice versa. But it might be 
interesting anyway - TR)

---------- Forwarded message ----------
Date: Thu, 03 Jan 2013 11:47:27 -0600
From: Brian Atkins <brian at posthuman.com>
To: transhumantech <tt at postbiota.org>
Subject: [tt] Promising compound restores memory loss and reverses symptoms of
    Alzheimer's (in mice)

http://www.eurekalert.org/pub_releases/2013-01/foas-pcr010213.php

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

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."

###

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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