Creating a free account will enable you to subscribe to our daily and weekly email newsletters, as well as customize your reading experience to show only the categories most relevant to you.
Signing up only take a few minutes, so why not give it a try and see what you've been missing out on.
Scientists from the Florida campus of The Scripps Research Institute have identified a critical regulator of a molecule deeply involved in the progression of Alzheimer's disease.
The new study, published in an advance, online edition of the Journal of Biological Chemistry, shows for the first time that levels of this regulating protein are decreased in the brains of Alzheimer's disease sufferers and that this decrease could be a significant factor in the advance of the disease.
The regulator is known as Rheb, a protein that many believe may be active in neural plasticity, the ability of the brain to change in response to learning.
In the new study, the scientists found that Rheb binds and regulates activity of a molecule known as BACE1, an important enzyme in Alzheimer's disease pathology, establishing for the first time a new molecular link between Rheb and BACE1.
"We found that Rheb regulates BACE1, which is a major drug target in Alzheimer's disease," said Srini Subramaniam, a TSRI biologist who led the study. "Studies of the autopsied brains of Alzheimer's patients have found a significant reduction in Rheb, so it is possible that an increase in Rheb could reverse the buildup of amyloid plaque."
The study noted that in some genetically modified animal models, an increase of Rheb has already been shown to reduce BACE1 levels and the production of amyloid plaque.
"If we can uncover the mechanism by which Rheb alters BACE1 levels, that would be a very good drug target," said Neelam Shahani, a first author of the study with William Pryor, both research associates in the Subramaniam lab.
The new study indicates that Rheb degrades BACE1 through a number of pathways, but more research needs to be done before drug candidates can be developed.
"We're very interested in the disease process and plan to keep moving forward to understand precisely how Rheb regulates BACE1," said Pryor.
Rheb GTPase Regulates β-Secretase Levels and Amyloid β Generation, Authors: Neelam Shahani; William Pryor; Supriya Swarnkar; Nikolai Kholodilov; Gopal Thinakaran; Robert E. Burke and Srinivasa Subramaniam, Journal of Biological Chemistry, Published on December 24, 2013, doi: 10.1074/jbc.M113.532713
Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our Alzheimer's / Dementia category page for the latest news on this subject.
Please use one of the following formats to cite this article in your essay, paper or report:
The Scripps Research Institute. "Scripps Florida scientists find regulator of amyloid plaque buildup in Alzheimer's disease." Medical News Today. MediLexicon, Intl., 27 Jan. 2014. Web.
21 Apr. 2014. <http://www.medicalnewstoday.com/releases/271679>
The Scripps Research Institute. (2014, January 27). "Scripps Florida scientists find regulator of amyloid plaque buildup in Alzheimer's disease." Medical News Today. Retrieved from
Please note: If no author information is provided, the source is cited instead.
If you write about specific medications, operations, or procedures please do not name healthcare professionals by name.
For any corrections of factual information, or to contact our editorial team, please use our feedback form. Please send any medical news or health news press releases to:
Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.
This page was printed from: http://www.medicalnewstoday.com/releases/271679.php
Visit www.medicalnewstoday.com for medical news and health news headlines posted throughout the day, every day.
© 2004-2014 All rights reserved. MNT is the registered trade mark of MediLexicon International Limited.