Se afișează postările cu eticheta Prevents. Afișați toate postările
Se afișează postările cu eticheta Prevents. Afișați toate postările

joi, 15 decembrie 2011

New Drug That Improves Memory And Prevents Brain Damage In Mice May Prevent Alzheimer's Disease Progression

Main Category: Alzheimer's / Dementia
Also Included In: Parkinson's Disease;  Huntingtons Disease;  Stroke
Article Date: 15 Dec 2011 - 7:00 PST

email icon email to a friend   printer icon printer friendly   write icon opinions  
not yet ratednot yet rated
A new drug candidate may be the first capable of halting the devastating mental decline of Alzheimer's disease, based on the findings of a study published in PLoS one.

When given to mice with Alzheimer's, the drug, known as J147, improved memory and prevented brain damage caused by the disease. The new compound, developed by scientists at the Salk Institute for Biological Studies, could be tested for treatment of the disease in humans in the near future.

"J147 enhances memory in both normal and Alzheimer's mice and also protects the brain from the loss of synaptic connections," says David Schubert, the head of Salk's Cellular Neurobiology Laboratory, whose team developed the new drug. "No drugs on the market for Alzheimer's have both of these properties."

Although it is yet unknown whether the compound will prove safe and effective in humans, the Salk researchers' say their results suggest the drug may hold potential for treatment of people with Alzheimer's.

As many as 5.4 million Americans suffer from Alzheimer's, according to the National Institutes of Health. More than 16 million will have the disease by 2050, according to Alzheimer's Association estimates, resulting in medical costs of over $1 trillion per year.

The disease causes a steady, irreversible decline in brain function, erasing a person's memory and ability to think clearly until they are unable to perform simple tasks such as eating and talking, and it is ultimately fatal. Alzheimer's is linked to aging and typically appears after age 60, although a small percentage of families carry a genetic risk for earlier onset. Among the top ten causes of death, Alzheimer's is the only one without a way to prevent, cure or slow disease progression.

Scientists are unclear what causes Alzheimer's, which appears to emerge from a complex mix of genetics, environment and lifestyle factors. So far, the drugs developed to treat the disease, such as Aricept, Razadyne and Exelon, only produce fleeting memory improvements and do nothing to slow the overall course of the disease.

To find a new type of drug, Schubert and his colleagues bucked the trend within the pharmaceutical industry of focusing exclusively on the biological pathways involved in the formation of amyloid plaques, the dense deposits of protein that characterize the disease. To date, Schubert says, all amyloid-based drugs have failed in clinical trials.

Instead, the Salk team developed methods for using living neurons grown in laboratory dishes to test whether or not new synthetic compounds were effective at protecting the brain cells against several pathologies associated with brain aging. Based on the test results from each chemical iteration of the lead compound, which was originally developed for treatment of stroke and traumatic brain injury, they were able to alter its chemical structure to make a much more potent Alzheimer's drug.

"Alzheimer's is a complex disease, but most drug development in the pharmaceutical world has focused on a single aspect of the disease - the amyloid pathway," says Marguerite Prior, a research associate in Schubert's lab, who led the project along with Qi Chen, a former Salk postdoctoral researcher. "In contrast, by testing these compounds in living cell cultures, we can determine what they do against a range of age-related problems and select the best candidate that addresses multiple aspects of the disease, not just one."

With a promising compound in hand, the researchers shifted to testing J147 as an oral medication in mice. Working with Amanda Roberts, a professor of molecular neurosciences at The Scripps Research Institute, they conducted a range of behavioral tests that showed that the drug improved memory in normal rodents.

The Salk researchers went on to show that it prevented cognitive decline in animals with Alzheimer's and that mice and rats treated with the drug produced more of a protein called brain-derived neurotrophic factor (BDNF), a molecule that protects neurons from toxic insults, helps new neurons grow and connect with other brain cells, and is involved in memory formation.

Because of the broad ability of J147 to protect nerve cells, the researchers believe that it may also be effective for treating other neurological disorders, such as Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis (ALS), as well as stroke.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our alzheimer's / dementia section for the latest news on this subject. The research was funded by the Fritz B. Burns Foundation, the National Institutes of Health, the Bundy Foundation and the Alzheimer's Association.
Salk Institute Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Salk Institute. "New Drug That Improves Memory And Prevents Brain Damage In Mice May Prevent Alzheimer's Disease Progression." Medical News Today. MediLexicon, Intl., 15 Dec. 2011. Web.
15 Dec. 2011. APA

Please note: If no author information is provided, the source is cited instead.


Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam)

Contact Our News Editors

For any corrections of factual information, or to contact the editors 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.



View the original article here

joi, 8 decembrie 2011

Long Non-Coding RNA Prevents The Death Of Maturing Red Blood Cells

Main Category: Biology / Biochemistry
Article Date: 08 Dec 2011 - 3:00 PST

email icon email to a friend   printer icon printer friendly   write icon opinions  
not yet ratednot yet rated
A long non-coding RNA (lncRNA) regulates programmed cell death during one of the final stages of red blood cell differentiation, according to Whitehead Institute researchers. This is the first time a lncRNA has been found to play a role in red blood cell development and the first time a lncRNA has been shown to affect programmed cell death.

"Programmed cell death, or apoptosis, is very important, particularly in the hematopoietic (blood forming) system, where inhibition of cell death leads to leukemias," says Whitehead Institute Founding Member Harvey Lodish, who is also a professor of biology and a professor of bioengineering at MIT. "We know a lot about the genes and proteins that regulate apoptosis, but this is the first example of a non-coding RNA that plays a role in blood cells. We would not be surprised to find this lncRNA or others like it upregulated in cancers."

And if an upregulated lncRNA is associated with cancer-cell survival, it may represent a new avenue of attack for therapeutics.

Currently, little is known about the specific function of lncRNAs, despite their abundance in cells. Only an estimated 10% of RNAs transcribed in a human cell go on to template proteins, according to a 2007 assessment of the human genome by the Encyclopedia of DNA Elements (ENCODE) Project Consortium, which was funded by the National Human Genome Research Institute. The rest of the RNAs are lumped together under the umbrella term "non-coding RNAs (ncRNAs)." Those longer than 200 base pairs are classified as lncRNAs.

LncRNAs were first identified in the 1980s. Currently about 100 lncRNAs have been studied in multiple types of mammalian tissues. LncRNAs have been shown to regulate gene expression by modifying chromatin, enhancing transcription, and promoting messenger RNA (mRNA) degradation as well as through other methods that have yet to be elucidated.

Despite increasing interest in and study of lncRNAs in a host of biological processes, this is the first research to identify a role for a specific lncRNA in erythropoiesis red blood cell production. This new lncRNA and its function are described this week in the online edition of the journal Genes and Development.

By examining fetal mouse livers, which are rich sources of red blood cells and their progenitors, Wenqian Hu screened the various stages of red blood cell development for the presence of lncRNAs. Hu, the first author of the Genes and Development paper and a postdoctoral researcher in Lodish's lab, found more than 400 lncRNAs expressed in these cells. During the end of the red blood cell maturation process, one lncRNA in particular was found to be highly expressed; the group dubbed this lncRNA "long intergenic non-coding RNA-erythroid-pro-survival" or lincRNA-EPS.

To determine its function, Hu halted expression of lincRNA-EPS in maturing red blood cells; the cells died as they began the differentiation process. Then Hu expressed lincRNA-EPS in maturing red blood cells and grew these cells in the absence of the hormone erythropoietin, which normally prevents the blood cell progenitors from undergoing apoptosis. Instead of dying as expected from the lack of erythropoietin, the cells with lincRNA-EPS continued to live, indicating that lincRNA-EPS by itself can prevent apoptosis.

After further investigation, Hu found that lincRNA-EPS inhibits the expression of Pycard, a gene that promotes programmed cell death, explaining in part lincRNA-EPS's role in apoptosis prevention.

"These experiments indicate that the normal function of this lncRNA is to protect the red blood cells from death during the last step of differentiation," says Hu. "This is important because the final step of red blood cell maturation is the expulsion of the nucleus from the cell, which in many ways mimics apoptosis. This lncRNA and other factors make sure the cell can get rid of the nucleus and differentiate properly and that it does not go through apoptosis."

Because programmed cell death goes awry in leukemias and other cancers, Hu is currently examining lincRNA-EPS's function in normal and diseased human cells in an effort to determine whether it plays a role in tumor development and growth.

This work was supported by the Life Sciences Research Foundation and the National Institutes of Health (NIH).

"Long non-coding RNA mediated anti-apoptotic activity in murine erythroid terminal differentiation"

Genes and Development online, December 8, 2011

Wenqian Hu (1), Bingbing Yuan (1), Johan Flygare (1,3), and Harvey F. Lodish (1, 2).

1. Whitehead Institute for Biomedical Research, Cambridge, MA, 02142, USA

2. Departments of Biology and Bioengineering, Massachusetts Institute of Technology, Cambridge, MA, 02142, USA

3. Present address: Division of Molecular Medicine and Gene Therapy, Lund University, BMC A12, 221 84 Lund, Sweden

Article adapted by Medical News Today from original press release. Source: Whitehead Institute for Biomedical Research
Visit our biology / biochemistry section for the latest news on this subject. Whitehead Institute for Biomedical Research Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Whitehead Institute for Biomedical Research. "Long Non-Coding RNA Prevents The Death Of Maturing Red Blood Cells." Medical News Today. MediLexicon, Intl., 8 Dec. 2011. Web.
8 Dec. 2011. APA

Please note: If no author information is provided, the source is cited instead.


Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam)

Contact Our News Editors

For any corrections of factual information, or to contact the editors 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.



View the original article here