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New obesity compound shows promise in mice

July 28, 2010 By vani Leave a Comment

(Reuters) – A compound similar to Sanofi-Aventis’ once-promising weight loss drug Acomplia helped obese mice lose weight and lower their blood fats and blood sugar without causing psychological side effects, U.S. researchers said on Monday.

Like Acomplia, the drug targets cannabinoid receptors that become active after smoking marijuana, but the team tinkered with the compound to keep it from crossing over into the brain, reducing the risk of depression, anxiety or other neurological problems seen in the original drug.

While obese mice do not lose as much weight on this new compound, it was just as effective as Acomplia in reducing obesity-related metabolic changes, researchers from the National Institutes of Health and Northeastern University reported in the Journal of Clinical Investigation.

“It does cause weight loss in diet-related obesity, but less than the other compound, which is not the only problem in obesity,” Dr. George Kunos of the NIH in Bethesda, Maryland, said in a telephone interview.

Obesity has become an epidemic in the United States, leading to a huge increase in diabetes and a host of related health problems. But many potential weight-loss drugs have either failed or been abandoned due to safety issues.

Acomplia had to be pulled from the market after it was linked to several deaths and hundreds of adverse drug reactions in Britain.

The drug, known generically as rimonabant, never won U.S. approval after a panel of experts rejected it amid fears it may cause suicidal thoughts.

Rimonabant targets the protein CB1R, the same molecule that controls the effects of marijuana. CB1R is present both in the brain and in organs such as the liver and pancreas and fat tissue.

Kunos and Alexandros Makriyannis of Northeastern University in Boston tested a more selective drug that only blocks CB1R in peripheral organs, but cannot get into the brain.

They found mice that become fat from eating too much lost about 12 percent of their body weight on this new formulation, compared with 21 percent in similar mice that had taken rimonabant.

But Kunos said the other effects — reduced blood fats that can cause heart disease and lower blood sugar that can affect the risk of diabetes — were about the same with both the new and the old drugs.

Kunos said the drug had no effect on mutant mice that were obese because they lacked the appetite-suppressing hormone leptin.

“In obesity, mice and humans lose their sensitivity to leptin. This drug restores that sensitivity,” Kunos said, offering a possible explanation for the difference.

He said the next step is to do tests to see if the drug is toxic to humans. Eventually, the hope is that the drug will be tested as a new anti-obesity treatment.

(Editing by Mohammad Zargham)

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Healthy older brains not smaller than younger ones

September 8, 2009 By admin Leave a Comment

Washington, Sept 8 (ANI): The belief that healthy older brains are substantially smaller than younger brains has been deemed incorrect by Dutch researchers.

The authors suggest that previous findings may have overestimated atrophy and underestimated normal size for the older brain.

The new study tested participants in Holland’s long-term Maastricht Aging Study who were free of neurological problems such as dementia, Parkinson’s disease or stroke.

Once participants were deemed otherwise healthy, they took neuropsychological tests, including a screening test for dementia, at baseline and every three years afterward for nine years.

MRI scans were used to measure seven different parts of the brain, including the memory-laden hippocampus, the areas around it, and the frontal and cingulate areas of the cognitively critical cortex.

The participants were later divided into two groups: one group with 35 cognitively healthy people who stayed free of dementia (average starting age 69.1 years), and the other group with 30 people who showed substantial cognitive decline but were still dementia-free (average starting age 69.2 years).

In contrast to the 35 people who stayed healthy, the 30 people who declined cognitively over study-period showed a significant effect for age in the hippocampus and parahippocampal areas, and in the frontal and cingulate cortices.

In short, among the people whose cognition got worse, older participants had smaller brain areas than younger participants.

Thus, the seeming age-related atrophy in gray matter more likely reflected pathological changes in the brain that underlie significant cognitive decline than aging itself, wrote the authors.

As long as people stay cognitively healthy, the researchers believe that the gray matter of areas supporting cognition might not shrink much at all.

If future longitudinal studies find similar results, our conception of ‘normal’ brain aging may become more optimistic,” said lead author Saartje Burgmans, who is due to receive her PhD later this year.

The study appears in journal Neuropsychology. (ANI)

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Novel minimally invasive surgery for treating spinal cancer patients

September 8, 2009 By admin Leave a Comment

Washington, Sep 8 (ANI): Doctors at Toronto Western Hospital have come up with a new minimally invasive, outpatient spine surgical procedure for treating cancer that has spread to the spine.

It is believed that almost 40-50 percent of metastic cancers end up in the spine and the most common primary cancers to spread to the bones of the spine are breast and lung cancer.

Spinal tumours can drastically affect a patient’s quality of life and result in pain and reduced mobility.

A spinal tumour or a growth of any kind can impinge on nerves, leading to pain, neurological problems and sometimes paralysis.

The new procedure involves a small incision in the back (the size of a loonie) in order to remove the tumour and stabilize the damaged spine.

Other than providing a shorter recovery time, its benefits also include allowing patients to receive radiation treatment shortly after surgery.

Traditional surgical methods involve a longer and more painful recovery process, thus making patients to wait weeks before resuming radiation treatment.

The combination of surgery and radiation leads to better outcomes and quality of life. (ANI)

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Bird flu virus strain leaves survivors at increased Parkinson’s disease risk

August 20, 2009 By admin Leave a Comment

Washington, August 20 (ANI): An animal study conducted by experts at St. Jude Children’s Research Hospital has suggested that at least one strain of the H5N1 avian influenza virus leaves survivors at significantly increased risk for Parkinson’s disease, and possibly other neurological problems later in life.

In their study report, the researchers write that mice that survived infection with an H5N1 flu strain were found to be more likely than uninfected mice to develop brain changes associated with neurological disorders like Parkinson’s and Alzheimer’s diseases.

Parkinson’s and Alzheimer’s involve loss of brain cells crucial to a variety of tasks, including movement, memory and intellectual functioning.

The researchers say that their study has shown that the H5N1 flu strain causes a 17 percent loss of the same neurons lost in Parkinson’s as well as accumulation in certain brain cells of a protein implicated in both diseases.

“This avian flu strain does not directly cause Parkinson’s disease, but it does make you more susceptible,” said Dr. Richard Smeyne, associate member in St. Jude Developmental Neurobiology.

“Around age 40, people start to get a decline in brain cells. Most people die before they lose enough neurons to get Parkinson’s. But we believe this H5N1 infection changes the curve. It makes the brain more sensitive to another hit, possibly involving other environmental toxins,” Smeyne added.

Smeyne revealed that the study focused on a single strain of the H5N1 flu virus, the A/Vietnam/1203/04 strain, and that the threat posed by other viruses, including the current H1N1 pandemic flu virus, was still being studied.

During the study, the researchers infected some mice with an H5N1 flu strain isolated in 2004 from a patient in Vietnam, which is still considered to be the most virulent of the avian flu viruses.

About two-thirds of the mice developed flu symptoms, primarily weight loss. After three weeks, there was no evidence of H5N1 in the nervous systems of the mice that survived.

However, the inflammation triggered by the infection within the brain continued for months, and it was found to be quite similar to inflammation associated with inherited forms of Parkinson’s.

Although the tremor and movement problems disappeared as flu symptoms eased, the researchers reported that 60 days later, mice had lost roughly 17 percent of dopamine-producing cells in SNpc, a structure found in the midbrain.

They also found evidence that the avian flu infection led to over-production of a protein found in the brain cells of individuals with both Alzheimer’s and Parkinson’s diseases.

“The virus activates this protein,” Smeyne said.

The study has been reported in the online early edition of the Proceedings of the National Academy of Sciences. (ANI)

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Genetic variations lined to brain size

August 19, 2009 By admin Leave a Comment

Washington, August 19 (ANI): In what may help improve the scientific understanding of autism and other neurological disorders, an international team of researchers have for the first time shown that natural variations in a specific gene influence brain structure.

Co-led by Scripps Research Institute scientists, the research grew out of a larger project called the Thematic Organized Psychosis (TOP) study, which was led by Ole Andreassen at Ullelval University Hospital and Institute of Psychiatry at the University of Oslo in Norway.

TOP called for using extensive magnetic resonance imaging (MRI) scanning of hundreds of patients, including many with severe mental disorders, in collaboration with Anders Dale of the University of California, San Diego (UCSD), School of Medicine.

In the current study, the researchers focused on a gene called MECP2 because it plays major roles in controlling brain development.

Past studies with mice have shown that MECP2 regulates the activity of a wide range of other genes important in brain development. Substantial mutations in the gene also cause the rare disease Retts syndrome, in which brain growth slows, leading to a range of debilitating neurological problems and mental retardation.

Previous studies have also linked MECP2 to autism.

Given its obvious import, Schork says: “This was a logical gene to target.”

During the study, the researchers explored whether common variations likely to have small effects individually in the MECP2 and surrounding region in the DNA of patients could be tied directly to the way a patient’s brain develops.

They found that indeed some of these variations, known as single-nucleotide polymorphisms (SNPs), did correlate well with various measures of a patient’s brain, though there was no identifiable tie between the variations and the mental disorders.

The closest connection they found was between two specific SNPs and lower surface area folds of the outer layer, or cortex, of the brain-the “grey matter,” which plays critical roles in thinking, language, memory, and other functions.

“So, those sorts of common variations actually do have some functional consequences that are dictating variations in brain size,” says Schork.

Interestingly, the pattern was only seen in males.

Schork and his colleagues say that because MECP2 has been linked to autism, there is a very real possibility that studying SNPs in autistic patients might reveal one or more that link to brain development problems. This could even illuminate possible paths for autism treatments, they say.

The researchers are also looking at possible connections between variations in other key genes and various brain regions.

Besides overall brain size, researchers believe that some neurological conditions might be tied to increases in the size of certain brain components, perhaps due to unidentified genetic mutations. This could prevent other components from growing to their full size due to the limited space inside a skull, preventing proper functioning.

“Who knows? This opens things up considerably. Now we can cast a much wider net and maybe rope in genes nobody had a clue about and discover something that otherwise wouldn’t have been known,” says Schork.

The study has been reported in an advance, online Early Edition of the Proceedings of the National Academy of Sciences (PNAS). (ANI)

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Exposure to second-hand smoke ‘ups dementia risk’

February 13, 2009 By admin Leave a Comment

London, Feb 13 (ANI): A new study has revealed that exposure to second-hand smoke could increase the risk of developing dementia and other neurological problems.

For the study, Dr David Llewellyn and his research team from the University of Cambridge, Peninsula Medical School and the University of Michigan, examined saliva samples from almost 5000 non-smoking adults over the age of 50 using data from the 1998, 1999 and 2001 waves of the Health Survey for England (HSE).

The samples were tested for cotinine – a product of nicotine that can be found in saliva for about 25 hours after exposure to second-hand smoke.

Participants in the study also provided a detailed smoking history. Never smokers and previous smokers were assessed separately.

The researchers used established neuropsychological tests to assess brain function and cognitive impairment.

These focused on memory function, numeracy and verbal fluency – for example naming as many animals in a minute. The results of the tests were added together to provide a global cognitive function score.

Participants whose scores were in the lowest 10 percent were defined as suffering from some level of cognitive impairment.

The authors argue that the link between second-hand smoke and cognitive impairment could be explained given that heart disease increases the risk of developing dementia and second-hand smoke exposure is known to cause heart disease.

The study is published on bmj.com. (ANI)

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Biochemical switch needed for nerve cells to respond to DNA damage identified

January 19, 2009 By Rajesh Leave a Comment

London, January 19 (ANI): Scientists at Emory University School of Medicine have announced the identification of a biochemical switch, which is required for nerve cells to respond to DNA damage.

The researchers say that their finding illuminates a connection between proteins involved in neurodegenerative disease and in cells’ response to DNA damage.

Most children who inherit the disease ataxia telangiectasia are rendered wheelchair-bound by the time they turn 10, because of neurological problems. Patients also have weakened immune systems and more frequent leukemias, and are more sensitive to radiation.

According to the researchers, the problem mainly results from mutations in the ATM (ataxia telangiectasia mutated) gene, which encodes an enzyme that controls cells’ response to and repair of DNA damage.

The researchers say that it is possible to turn on ATM by treating cells with chemicals that damage DNA. Once other proteins in the cell detect broken DNA needing repair, they say, the ATM protein could activate itself directly.

The team have shown that an additional step is necessary first.

“In neurons that are not dividing anymore, we now know that another regulator is involved: Cdk5,” Nature Cell Biology quoted says Dr. Zixu Mao, associate professor of pharmacology and neurology at Emory University School of Medicine, as saying.

Mao and his colleagues have found that the Cdk5 protein must activate ATM before the gene can do its job in neurons.

Based on their findings, the researchers came to the conclusion that Cdk5 may be a potential drug target.

Cdk5 contributes to normal brain development, and aberrant Cdk5 activity is known to be involved in the death of neurons in several neurodegenerative diseases, including Alzheimer’s, Parkinson’s and amyotrophic lateral sclerosis.

“Cdk5 has a complex character. It can be bad for neurons if its activity is either too high or too low,” Mao says.

Mao revealed that his team were intrigued by reports that in these diseases, neurons that had stopped dividing appear to restart that process, copying their DNA, before dying.

“That’s what really kicked us into high gear,” he says.

The same process, called mitotic catastrophe, occurs when neurons suffer DNA damage. Inhibiting either Cdk5 or ATM can reduce the number of neurons that suffer mitotic catastrophe after DNA damage, the authors found. (ANI)

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