Molecular Biology

Pathway discovered to influence fat accumulation

Mon, 02 Jul 2007 20:01:39 -0400

In a remarkable breakthrough for weight research, scientists have reported the discovery of a neurochemical pathway that stimulates the accumulation of fat in animals laboring under chronically high stress and exposed to a diet of junk food. Inhibiting the pathway prevented weight gain in mice but selectively spurring the mechanism allowed for the strategic accumulation of weight--potentially opening a new pathway to mold larger breasts, firmer buttocks and younger faces.

Zofia Zukowska of Georgetown University's Department of Physiology and Biophysics led the project, which involved an international team of scientists. Researchers say their work may show that a confluence of high rates of stress and easy access to junk food has led to an epidemic of obesity. Mice in the study were left standing in cold water or exposed to an alpha mouse for part of each day and then offered either a junk food diet or standard feed. The mice receiving high fat diets swiftly added weight. An examination of their fat tissue revealed neuropeptide Y (NPY), a chemical messenger that is produced by the body's nerves. They also had extraordinarily high levels of the far higher levels of neuropeptide Y2R receptor, a molecular partner NPY needs in order to work.

- see the release on their work
- read the article from The Washington Post

ALSO: Mayo Clinic researchers have that the absence of the CD38 gene prevented mice on high-fat diets from gaining weight. Report

Related Articles:
A biologic mechanism for weight gain. Report
Scripps researchers find anti-obesity vaccine. Report
Molecular research points to new obesity therapy. Report
Scientists explore role of PYY in obesity. Report

New approaches pursued on Parkinson's

Mon, 25 Jun 2007 20:01:39 -0400

A team of scientists say they have developed a drug that blocks the SIRT2 enzyme, which protects the neurons damaged by Parkinson's disease. In an article to come out this week in the journal Science, researchers at Harvard show how inhibition of SIRT2--a member of the sirtuin family, which is linked to aging--prevents the toxicity of the protein aggregates that are believed to be behind the neuronal death characteristic of PD. Contrary to "classic" approaches that try to eliminate these aggregates, SIRT2 inhibition appears to work by "fusing" many small protein aggregates into larger (apparently less neuro-toxic) ones.

In addition, researchers at New York-Presbyterian Hospital/Weill Cornell Medical Center have also used an AAV virus to deliver a gene to the brains of 11 volunteers with Parkinson's disease. The gene is a regulator of GABA, a neurotransmitter. There were no side effects from the therapy and the treatment helped reduce the symptoms of Parkinson's for up to four years.

- see the release on SIRT2
- check out the report from the Daily Herald
- here's the report on AAV work

Related Articles:
Stem cell transplant a success against Parkinson's. Report
NIH researchers study genetic variations in Parkinson's disease. Report

MIT scientists reverse autism, retardation in mice

Mon, 25 Jun 2007 20:01:39 -0400

Researchers from the Picower Institute for Learning and Memory at Massachusetts Institute of Technology have reversed mild retardation and severe autism in mice by inhibiting the enzyme called p21-activated kinase (PAK). Their study focused on Fragile X Syndrome (FXS)--a leading cause of retardation and autism--which is linked to a mutated X chromosome gene. The PAK enzyme controls the connections between neurons and the brain.

"Strikingly, PAK inhibition also restored electrical communication between neurons in the brains of the FXS mice, correcting their behavioral abnormalities in the process," co-author Susumu Tonegawa, 1987 Nobel laureate and Picower Professor of Biology and Neuroscience, said in a prepared statement. "Notably, due to an elegant genetic manipulation of method employed by the Picower Institute researchers, PAK inhibition in the FXS mice did not take place until a few weeks after appearance of disease symptoms. This implies that future treatment may still be effective even after symptoms are already pronounced."

- read the report from Forbes

Related Article:
Potential breakthrough made for Down syndrome. Report

Big pharma sees big payback for Alzheimer's research

Mon, 11 Jun 2007 20:01:39 -0400

Wyeth has devoted more than 350 scientists to 23 separate research projects aimed at treating Alzheimer's. So far, that commitment has cost the giant drug developer more than $450 million. But while it's one of the most ambitious research projects in the world related to Alzheimer's, The New York Times concludes that a broad array of pharma and biotech companies are also looking for new therapies to treat a disease that is expected to claim millions of more victims as the populations of developed countries age. There's a payback at the end of that research. An effective treatment could command $20,000 a year per patient, making any possible approval a sure-fire blockbuster for years to come.

- read the report from The New York Times

ALSO: Alzheimer's disease researchers may be able to reduce the time and expense associated with clinical trials, according to early results from the Alzheimer's Disease Neuroimaging Initiative, a public-private research partnership organized by the National Institutes of Health. Release

Related Articles:
Researchers tout results for new Alzheimer's test. Report
Alzheimer's patch used to deliver vaccine to mice. Report

Universities, public institutes lead biotech revolution

Mon, 07 May 2007 20:01:39 -0400

A worldwide analysis of biotech patents shows that universities and public research institutions play the leading role in drug discovery, with the U.S. and Japan well ahead of Europe in innovation. The intellectual property firm Marks & Clerk examined patents filed between 2002 and 2006 and found that the Japan Science and Technology Agency played the lead role in filing 1,022 patent "families;" clusters of patents all linked to a single discovery. The University of California ranked second, with 543 patent families, and the U.S. government came in third, with 443 patent families--most coming from the National Institutes of Health. Their figures were presented at BIO 2007 in Boston this week.

Only a small number of private companies penetrated the firm's top-20 list. Genentech ranked fourth with 421 patent families while Millennium Pharmaceuticals came in sixth. In addition, the most high-profile patents were filed by universities, with the Massachusetts Institute of Technology holding all or part of the three most frequently cited patents. Europe fared poorly in the comparison. The universities of Texas, Pennsylvania, Florida, Johns Hopkins, Stanford and Columbia all held more than twice as many patent families as Oxford, the leading European university. Somewhat surprisingly, Denmark was the leading European country for biotech innovation while the 162 patent families created by the country's Novozymes put it at the top of the list of European companies.

- read the report from The Financial Times

Related Articles:
Milken ranks the world's top bioresearch colleges. Report
NIH program to create academic research consortium. Report

Gene deletion study defuses disease risk from fat

Mon, 07 May 2007 20:01:39 -0400

A new study in mice raises the possibility that humans may one day be able to eat any kind of fat they want without raising their risk of heart disease. The study involved deleting a gene in the mice that causes production of ACAT2, an enzyme that alters the molecular structure of cholesterol so that it can be transported to the body's cells.

"We deleted an enzyme in mice and they could eat any type of fat and not get heart disease," said Lawrence Rudel, Ph.D., a professor of comparative medicine. "If you're a mouse, it's great. Of course, we don't know yet if it will be the same in humans."

- read the release for more information

Related Articles:
Drug switches on fat-burning gene in mice. Report
Molecular research points to new obesity therapy. Report
Scripps researchers find anti-obesity vaccine. Report
A biologic mechanism for weight gain. Report

Cells prompted to "eat" Huntington proteins

Mon, 07 May 2007 20:01:39 -0400

Scientists have developed a novel strategy for tackling neurodegenerative diseases such as Huntington's disease: encouraging an individual's own cells to "eat" the malformed proteins that lead to the disease. Professor David Rubinsztein, Wellcome Trust Senior Clinical Fellow at the University of Cambridge, has been studying the molecular biology underlying Huntington's and other neurodegenerative diseases. Huntington's occurs when a protein known as huntingtin builds up in the brain cells of patients, mainly in neurons in the basal ganglia and in the cerebral cortex. Normally, cells dispose of or recycle their waste material, including unwanted or mis-folded proteins, through a process known as autophagy, or "self-eating".

"We have shown that stimulating autophagy in the cells--in other words, encouraging the cells to eat the malformed huntingtin proteins -- can be an effective way of preventing them from building up," says Professor Rubinsztein. "This appears to stall the onset of Huntington's-like symptoms in fruit fly and mice, and we hope it will do the same in humans."

- read the report on the research study

Related Articles:
Mayo researchers find trigger for Huntington's. Report
Huntington's study reveals insights on genetic testing. Report
New agent disables genetic diseases. Report

A new compound to treat Alzheimer's

Mon, 23 Apr 2007 20:01:39 -0400

A researcher at Purdue University laboratory is working on a compound that he says could become the first treatment available for Alzheimer's. Arun Ghosh says the molecule targets an enzyme called memapsin 2, or beta-secretase, which plays a key role in the formation of beta amyloid plaque that is widely believed to be responsible for the disease. Ghosh used X-ray crystallography to map the structure of an inhibitor he designed that was bound to the enzyme. Ghosh formed a company with Jordan Tang, head of the Protein Studies Research Program at the Oklahoma Medical Research Foundation, which has merged with CoMentis in San Francisco.

"The moment we had the crystal structure, we knew exactly how the inhibitor worked, the interactions of the molecular bonds and what properties were most important," Ghosh said. "This allowed us to quickly build inhibitor molecules and bypass the usual lengthy process of trial and error in molecule design. Within a year we had developed modified inhibitors that were much smaller and more drug-like in character."

"This is the most exciting target today for Alzheimer's disease intervention," said Tang, who holds the J.G. Puterbaugh Chair in Medical Research at the Oklahoma Medical Research Foundation. "These interactions happen at a very early stage in the disease, and if we could block them, we could prevent many of the harmful steps that follow and drastically reduce the impact. In our most recent tests, a single dose of the designed compound reduced the beta-amyloid level by 30 percent."

- check out the release
- here's the report on their work from the Indianapolis Star

ALSO: A type of omega-3 fatty acid may slow the growth of two brain lesions that are hallmarks of Alzheimer's disease, UC Irvine scientists have discovered. The finding suggests that diets rich in docosahexaenoic acid can help prevent the development of Alzheimer's disease later in life. Release

PLUS: Scientists know little about how the brain chooses cells to encode and store memories. Now a UCLA-University of Toronto team has discovered that a protein called CREB controls the odds of a neuron participating in memory formation. Release

Related Articles:
Existing drugs could fight Alzheimer's. Report
Researchers hopeful of Alzheimer's cure. Report
Researchers discovers new class of Alzheimer's drug. Report

Scripps team finds path to synthesizing natural compounds

Mon, 26 Mar 2007 20:01:39 -0400

A research team at Scripps Research Institute has discovered a simpler, less expensive method for producing synthetic versions of naturally-occurring compounds. Scripps researcher Phil Baran and a couple of graduate students at Scripps Research Kellogg School of Science and Technology say they were able to eliminate a step in the process. By making it possible to produce these compounds less expensively, they say that a number of new drugs could be much more feasible to make. And that would allow for commercialization of active ingredients found in marine and terrestrial organisms.

Their work points the way to avoiding reliance on "protecting groups," which are extra compounds chemists use to shield reactive portions of a molecule during specific stages of a synthesis scheme. The protecting groups are eventually cleaved chemically to expose the reactive portion during later chemical reactions to complete a product's synthesis. Each protecting group used adds at least two steps to a synthesis, and the groups themselves have reactivity of their own that must be controlled to prevent adverse reactions. To avoid the need for protecting groups, the Baran group took an unorthodox approach. Rather than assume that reactive portions of a molecule had to be shielded during various syntheses, the researchers calculated ways to use such reactivity in an overall scheme to produce the desired final product.

- here's the release for more information
- read the report on the Scripps' research from Tech Journal South

Related Articles:
Scripps researchers find anti-obesity vaccine. Report
Scripps Florida sees first biotech spinoff take root. Report
Scripps inks $100M research pact with Pfizer. Report

Anesthetics can spur brain plaque

Mon, 12 Mar 2007 20:01:39 -0400

A class of widely used anesthetics spurs production of beta amyloid in the brains of mice, according to a study completed at the University of Pennsylvania. Researchers studied halothane, one in a class of volatile anesthetics used on 60 million people a year. A common side effect of these anesthetics is 'post-operative cognitive decline' that can last from days to years. If the drugs also promote beta amyloid in the brains of humans, it could provide a direct link to Alzheimer's. While there is no conclusive proof that beta amyloid causes Alzheimer's, the presence of brain plaque is a common feature of the disease. Researchers in the field have been pushing an array of drug development programs that target beta amyloid.

- here's the report on the study from Nature

Related Articles:
Scientists induce brain disorders in Alzheimer's mice. Report
Enzyme essential to preventing Alzheimer's. Report