 HOW FATS GET TRAPPED
Swedish researchers discover protein that stimulates formation of fat cells
Closing in on a better treatment for schizophrenia
PARIS
Scientists looking at the effects of LSD in the brain have made an unexpected discovery that could lead to better treatment for schizophrenia.
While investigating how hallucinogens change brain chemistry, a team of researchers led by Stuart Sealfon at the Mount Sinai School of Medicine in New York noticed that the neural pathways affected, as well as key symptoms, were very similar to those in schizophrenia patients.
Schizophrenics often hear voices, and may believe that other people are reading their minds or controlling their thoughts. These frightening experiences can cause social withdrawal and extreme agitation. There is no known cure for the chronic disorder, which affects approximately one in 200 people, emerging in men in their late teens and early 20s, and a decade later in women, according to the World Health Organization.
Created by a Swiss chemist in the late 1930s as a possible treatment for neural and respiratory troubles, lysergic acid diethylamide (LSD) emerged in the 1950s and 1960s as a popular recreational drug. LSD influences the same serotonin receptors that are unbalanced in schizophrenics, and both the drug and the disease result in delusions and hallucinations.
In experiments on mice, Sealfon also found that LSD-in order to produce the effects sought after-must simultaneously act on a receptor regulating glutamate, the principal excitatory neurotransmitter. "While the LSD is binding to the serotonin part of this complex, it takes glutamate and serotonin together to create the unique changes in the cell that occur with LSD," Sealfon said.
When mice under the influence of LSD were given a second drug targeting only the glutamate receptor, it neutralized the hallucinogenic effect of the LSD, said the study published in Nature. This is significant, explained Sealfon, in light of a recent breakthrough treatment for schizophrenia that-unlike any previous drugs-acts only on the glutamate receptors.
A study published recently on successful clinical trials "was international news because it was the first completely new approach to schizophrenia in decades," he said.
An older class of so-called atypical antipsychotic drugs acts exclusively on serotonin levels, but Sealfon's findings suggest that-like LSD-the abnormal brain chemistry in schizophrenics may require medicines that regulate both at once.
Autopsies of schizophrenic patients who had been treated with any of the atypical antipsychotic drugs show normal serotonin levels, but low glutamate, he pointed out. "This could lead to identifying new kinds of drugs to treat schizophrenia that act on this serotonin-glutamate complex," said Sealfon, adding that his research was not originally designed to investigate the disease.
His study also helps settle a decades-long debate, providing further evidence that LSD does, in fact, mirror the symptoms and chemical activity found in the brains of schizophrenics.
Antiageing substance found in bullfrogs
SEOUL
While it only turns into a handsome prince in fairy tales, the homely bullfrog may harbor a valuable antiageing substance for humans. A team led by Prof. Kim Se-kwon of Pukyong University in Busan says they isolated a peptide with antioxidant properties from bullfrog skin. Because of the properties, the material is useful in removing free radicals-molecules that hasten the ageing process of human cells.
Alpha-tocopherol is traditionally considered as the most active antioxidant in humans and widely used in medicines and health supplements. But its price keeps rising because of surging world demand.
"The new substance can provide an economic alternative to tocopherol," Kim said, referring to another antioxidant. The team's discovery was published by Bioresource Technology last year. "Because it is water-soluble, the substance may be consumed in much more diverse ways than the oil-soluble tocopherol. You may put it in soft drinks, for example," he said. The newly found material is also 10-percent more efficient than tocopherol in curbing oxidation, he added.
Alzheimer's risk skyrockets when both parents diagnosed
CHICAGO
The risk of developing Alzheimer's disease skyrockets when both parents are struck by the degenerative brain disorder. The dementia also seems to strike at an earlier age among patients with a wide family history of the disease, a study published in the Archives of Neurology found.
"Because Alzheimer disease is so common in the general population, it is not uncommon for both spouses to develop the disease," wrote lead author Suman Jayadev of the University of Washington, Seattle. "Offspring of two such affected individuals would presumably carry a higher burden of these Alzheimer's disease-associated genes."
Jayadev and her colleagues studied the frequency of Alzheimer's disease in adult children of 111 families in which both parents had been clinically diagnosed with the disease. They found that of the 297 offspring who reached adulthood, 22.6 percent developed Alzheimer's disease compared with an estimated six to 13 percent of the general population.
But since 79 percent of those still untouched by the disease had not yet reached the age of 70, it is likely that the actual risk is higher, the authors concluded. That's because they found that the risk of developing the disease increased with age: 31 percent of those older than age 60 and 41.8 percent of those older than age 70 had been diagnosed with Alzheimer's. At age 80, the cumulative risk was determined to "beyond 60 percent."
The presence of Alzheimer's disease elsewhere in the family did not seem to increase the likelihood of developing the disease. But it was linked to an earlier onset: those whose family history of Alzheimer's was limited to their parents had an average onset of 72 years; those who had one parent with a family history of Alzheimer's had an average onset of 60 years; and those with a history of Alzheimer's on both sides of their family had an average onset of 57 years.
Protein that could fight obesity discovered
STOCKHOLM
A team of researchers in Sweden has discovered a protein that stimulates the formation of fat cells, a finding that could potentially be used to treat obesity. The protein called TRAP (tartrate-resistant acid phosphatase), "stimulates the formation of new fat cells and can thus precipitate the development of obesity," said the Karolinska Institute.
The research was based on cell cultures and mice studies, and showed that patients with obesity have excessive levels of the protein.
"This protein is potentially useful in the treatment of conditions involving morbid cachexia, such as cancer diseases," said Prof. Goeran Andersson, who led the study. "The discovery can also lead to new ways of treating obesity based on the inhibition of this protein's effect."
The study, which lasted four years and followed 14 obese women, was published in the US online journal Public Library of Science.
Chronic-fatigue syndrome linked to glandular fever
SYDNEY
Australian researchers have linked chronic-fatigue syndrome, a mystery affliction that has long puzzled scientists, with temporary brain injuries caused by glandular fever.
Sufferers of the debilitating syndrome, which can leave them listless and unable to carry out everyday tasks for months or even years, have often been dismissed by the unsympathetic as malingerers.
But researchers at the University of New South Wales said they had found the condition was not caused by a virus or immune problems, but from damage to the brain.
It is hoped the discovery will help scientists develop a treatment that works. At present, there is no cure or effective remedy for the syndrome, which is believed to affect up to 100,000 Australians.
The researchers carried out a seven-year study of 39 people with acute glandular fever caused by an infection called the Epstein-Barr virus.
In an article published in the Journal of Infectious Diseases, they said that eight of the subjects went on to develop chronic-fatigue syndrome.
They found the syndrome was not caused simply by exposure to the Epstein-Barr virus and it was not a result of an abnormal immune response by the patients. Other potential causes including neuroses and psychological disorders such as depression were also ruled out as causes of the condition.
Head researcher professor Andrew Lloyd said the study suggested some patients suffered brain injuries soon after contracting glandular fever and never fully recovered from the disease. The lingering symptoms were then diagnosed as chronic-fatigue syndrome.
"We believe that the parts of the brain that control perception of fatigue and pain get damaged during the acute-infection phase of glandular fever," he said.
"If you're still sick several weeks after infection, it seems that the symptoms aren't being driven by the activity of the virus in the body, it's happening in the brain."
Lloyd's research team is now attempting to prove the theory with sophisticated neurological tests and brain imaging technology.
"It's not too big a leap of faith to say after that, it's in the brain, because of the nature of the symptoms-it's fatigue, it's pain, sleep disturbance, concentration and memory difficulties and mood disturbance. They're very much brain symptoms," he said.
Lloyd said the study's ultimate goal was to discover the cause of chronic-fatigue syndrome and find a treatment that works. He said about 40 scientific trials on various treatments including anti-depressants, multivitamins, antiviral drugs, and immunological therapies had all failed to cure the condition.
Lloyd said that rehabilitation-style therapies such as graded exercise were the only treatments that had so far been shown to help alleviate symptoms.
He said chronic-fatigue sufferers often felt stigmatized and were accused of malingering because people did not believe their condition was real.
"I personally have never had a doubt that it's real because there are people who have got a set of symptoms that are unexplained," he said. "The real versus not real thing is often caught up in the mistaken notion about malingering or it's all depression but really there's no evidence to support that."
Moderate drinkers the least suicidal
TOKYO
Teetotalers and heavy drinkers face a greater risk of suicide than moderate drinkers. Heavy drinkers and men who never have a drop both commit suicide at 2.3 times the rate of those who enjoy only a few drinks a month, said a study released by Japan's health ministry. Heavy drinkers were classified as men who knocked back the equivalent of six glasses of wine or three double-shots of whisky a day more than once a week.
However, the researchers cautioned that drinking more moderately would not necessarily decrease the risk of suicide, as other factors like stress were also important. Also, some teetotalers are recovered alcoholics.
"Those who quit drinking may have done so for reasons such as severe illness or depression," Akechi Tatsuo, associate professor at Nagoya City University Medical School, wrote in the paper.
The study conducted by Tatsuo and other researchers looked at the behavior of 43,000 men between age 40 and 60 across Japan for a decade from 1990. A total of 168 of the men in the study committed suicide.
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