[net-gold] MEDICAL: RESEARCH : MEDICAL: CONDITIONS: DEMENTIA: Mental Decline Thwarted in Aging Rats
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- Date: Mon, 27 Sep 2010 00:19:16 -0400 (EDT)
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MEDICAL: RESEARCH:
Mental Decline Thwarted in Aging Rats
Date: Thu, 8 Jul 2010 13:11:11 -0400
From: "NIH OLIB (NIH/OD)" <olib@xxxxxxxxxx>
To: NIHPRESS@xxxxxxxxxxxx
Subject: Mental Decline Thwarted in Aging Rats
U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Institute of Mental Health (NIMH)
<http://www.nimh.nih.gov/>
Embargoed for Release: Thursday, July 8, 2010, 12 p.m. EDT
CONTACTS:
Jules Asher
NIMH press office
301-443-4536
e-mail:
NIMHpress@xxxxxxx
Karen Silver
NIH DPCPSI
301-435-2435
e-mail:
silverk@xxxxxxxxxxxx
MENTAL DECLINE THWARTED IN AGING RATS
NIH Grantees Eye Neuroprotective Mechanism for Alzheimer's
Scientists have discovered a compound that restores the capacity to form
new memories in aging rats, likely by improving the survival of newborn
neurons in the brain's memory hub. The research, funded in part by the
National Institutes of Health, has turned up clues to a neuroprotective
mechanism that could lead to a treatment for Alzheimer's disease.
"This neuroprotective compound, called P7C3, holds special promise because
of its medication-friendly properties," explained Steven McKnight, Ph.D.,
who co-led the research with Andrew Pieper, M.D., Ph.D., both of
University of Texas Southwestern Medical Center, Dallas. "It can be taken
orally, crosses the blood-brain barrier with long-lasting effects, and is
safely tolerated by mice during many stages of development."
The researchers report on their findings July 9, 2010 in the journal Cell.
Their work was funded, in part, by the NIH's National Institute of Mental
Health (NIMH), a NIH Director's Pioneer Award
http://commonfund.nih.gov/pioneer/Profiles04/McKnight.aspx
supported through the Common Fund
http://nihroadmap.nih.gov/
and managed by the National Institute of General Medical Sciences, and
National Cancer Institute.
"This striking demonstration of a treatment that stems age-related
cognitive decline in living animals points the way to potential
development of the first cures that will address the core illness process
in Alzheimer's disease," said NIMH Director Thomas Insel, M.D.
Physical activity, social, or other enriching experiences promote
neurogenesis -- the birth and maturation of new neurons. This growth takes
place in the dentate gyrus, a key area of the brain's memory hub, the
hippocampus. But even in the normal adult brain, most of these newborn
neurons die during the month it takes to develop and get wired into brain
circuitry. To survive, the cells must run a gauntlet of challenges.
Newborn hippocampus neurons fare much worse in aging-related disorders
like Alzheimer's, marked by runaway cell death.
In hopes of finding compounds that might protect such vulnerable neurons
during this process, Pieper, McKnight and colleagues tested more than 1000
small molecules in living mice. One of the compounds, designated P7C3,
corrected deficits in the brains of adult mice engineered to lack a gene
required for the survival of newborn neurons in the hippocampus. Giving
P7C3 to the mice reduced programmed death of newborn cells -- normalizing
stunted growth of branch-like neuronal extensions and thickening an
abnormally thin layer of cells by 40 percent. Among clues to the mechanism
by which P7C3 works, the researchers discovered that it protects the
integrity of machinery for maintaining a cell's energy level.
The html version of this release contains the image:
http://www.nimh.nih.gov/images/news-items/compound-mouse.jpg
To find out if P7C3 could similarly stem aging-associated neuronal death
and cognitive decline, the researchers gave the compound to aged rats.
Rodents treated with P7C3 for two months significantly outperformed their
placebo-treated peers on a water maze task, a standard assay of
hippocampus-dependent learning. This was traced to a threefold
higher-than-normal level of newborn neurons in the dentate gyrus of the
treated animals. Rats were used instead of mice for this phase of the
study because the genetically engineered mice could not swim.
The researchers pinpointed a derivative of P7C3, called A20, which is even
more protective than the parent compound. They also produced evidence
suggesting that two other neuroprotective compounds eyed as possible
Alzheimer's cures may work through the same mechanism as P7C3. The A20
derivative proved 300 times more potent than one of these compounds
currently in clinical trials for Alzheimer's disease. This suggested that
even more potent neuroprotective agents could potentially be discovered
using the same methods. Following up on these leads, the researchers are
now searching for the molecular target of P7C3 -- key to discovering the
underlying neuroprotective mechanism.
The html version of this release contains the image:
http://www.nimh.nih.gov/images/news-items/
McKnightNeuroprotectiveRatDentateGyrus.jpg
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-----------------------------------------
REFERENCE:
Discovery of a Pro-neurogenic, Neuroprotective Chemical.
Pieper AA, Xie S, Capota E, Estill SJ, Zhong J, Long JM, Becker GL,
Huntington P, Goldman SE, Shen CH, Capota M, Britt JK, Kotti T, Ure K,
Brat DJ, Williams NS, MacMillan KS, Naidoo J, Melito L, Hsieh J, Brabander
JD, Ready JM, McKnight SL.
2010, Jul 8. Cell
##
This NIH News Release is available online at:
http://www.nih.gov/news/health/jul2010/nimh-08.htm
Sincerely,
David Dillard
Temple University
(215) 204 - 4584
jwne@xxxxxxxxxx
http://daviddillard.businesscard2.com
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