‘Superfood’ celery combats brain diseases

Celery may not only be good for diets but also help safeguard mental health. Researchers have found that it generates compounds that can fight Alzheimer’s and other degenerative diseases.

The compounds luteolin and diosmin appear to block the inflammation that causes the brains of victims to start shrinking and dying. In animal experiments they reduced the levels of amyloid beta, which forms the sticky deposits that build up in the brains of patients with Alzheimer’s.

The chemicals belong to a group of plant-based compounds known as flavonoids. “Luteolin and diosmin could be used in purified form as therapeutic agents,” said Dr Terrence

Town of Cedars-Sinai Medical Center, Los Angeles. “The compounds have few side effects and are available as dietary supplements.”

Any finding that celery may slow the progress of brain diseases could push it into the “superfood” bracket along with green peppers, camomile and other green vegetables that contain similar chemicals.

Town emphasised that research was in its early stages and based on animal experiments. His study used mice genetically modified to develop Alzheimer’s. Progress of the disease slowed sharply in animals given diosmin.

Dr Susanne Sorensen, of the Alzheimer’s Society, said: “We know a healthy balanced diet can reduce dementia risk. This work reinforces the need to eat a diet rich in fruit and vegetables.”

Treatments for diseases such as Alzheimer’s are becoming increasingly urgent. There are currently 700,000 people with dementia in the UK, at least 15,000 of whom are under 65, and some in their forties.

Key Mechanism in Development of Nerve Cells Found

ScienceDaily
Wed, 30 Sep 2009
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Chaos brews in the brains of newborns: the nerve cells are still bound only loosely to each other. Under the leadership of Academy Research Fellow Sari Lauri, a team of researchers at the University of Helsinki has been studying for years how a neural network capable of processing information effectively is created out of chaos. The team has now found a new kind of mechanism that adjusts the functional development of nerve cell contacts.

The results were published in early September as the leading article of the Journal of Neuroscience.

The work carried out by Lauri's team and its partners at the Viikki campus sheds light on a development path that results in some of the large number of early synapses becoming stronger. The researchers found out hat the BDNF growth factor of nerve cells triggers a functional chain which promotes the release of the neurotransmitter glutamate. BDNF enables the release of glutamate by prohibiting the function of kainate receptors which slow down the development of the preforms of the synapses. The activity of the kainate receptors restricts the release of glutamate and the development of synapses into functional nerve cell contacts.

It is noteworthy that the brain of a newborn itself seems to organise its own development. The electrical activity of the waking brain triggers the series of events controlled by the BDNF protein, as a result of which kainate receptor activity disappears in some synapses. The development is based on the considerable plasticity of the developing neural network: it can reshape its structureand function to a large extent.

According to Lauri, the new research results help understand how central nervous system diseases originating in early development are established. The finding also provides researchers with the opportunity to obtain information about the different aspects of endogenous activity of the brain. At the same time, it could be possible to develop new kinds of pharmaceuticals for the treatment of childhood epilepsy, for example.

Lauri's team conducted the research in co-operation with the research teams of Eero Castren and Tomi Taira from the Neuroscience Centre, and the research team of Jari Yli-Kauhaluoma from the Faculty of Pharmacy.

Scientists Make Paralyzed Rats Walk Again After Spinal-Cord Injury

Medical News Today
Mon, 21 Sep 2009

UCLA researchers have discovered that a combination of drugs, electrical stimulation and regular exercise can enable paralyzed rats to walk and even run again while supporting their full weight on a treadmill.

Published Nov. 20 in the online edition of Nature Neuroscience, the findings suggest that the regeneration of severed nerve fibers is not required for paraplegic rats to learn to walk again. The finding may hold implications for human rehabilitation after spinal cord injuries.

"The spinal cord contains nerve circuits that can generate rhythmic activity without input from the brain to drive the hind leg muscles in a way that resembles walking called 'stepping,'" explained principal investigator Reggie Edgerton, a professor of neurobiology and physiological sciences at the David Geffen School of Medicine at UCLA.

"Previous studies have tried to tap into this circuitry to help victims of spinal cord injury," he added. "While other researchers have elicited similar leg movements in people with complete spinal injuries, they have not achieved full weight-bearing and sustained stepping as we have in our study."

Edgerton's team tested rats with complete spinal injuries that left no voluntary movement in their hind legs. After setting the paralyzed rats on a moving treadmill belt, the scientists administered drugs that act on the neurotransmitter serotonin and applied low levels of electrical currents to the spinal cord below the point of injury.

The combination of stimulation and sensation derived from the rats' limbs moving on a treadmill belt triggered the spinal rhythm-generating circuitry and prompted walking motion in the rats' paralyzed hind legs.

Daily treadmill training over several weeks eventually enabled the rats to regain full weight-bearing walking, including backwards, sideways and at running speed. However, the injury still interrupted the brain's connection to the spinal cord-based rhythmic walking circuitry, leaving the rats unable to walk of their own accord.

Neuro-prosthetic devices may bridge human spinal cord injuries to some extent, however, so activating the spinal cord rhythmic circuitry as the UCLA team did may help in rehabilitation after spinal cord injuries.

The study was funded by the Christopher and Dana Reeve Foundation, Craig Nielsen Foundation, National Institute of Neurological Disorders and Stroke, U.S. Civilian Research and Development Foundation, International Paraplegic Foundation, Swiss National Science Foundation and the Russian Foundation for Basic Research Grants.

Antioxidant Controls Spinal Cord Development

PhysOrg
Fri, 18 Sep 2009 13:55 UTC

Researchers at the Johns Hopkins School of Medicine have discovered how one antioxidant protein controls the activity of another protein, critical for the development of spinal cord neurons. The research, publishing this week in Cell, describes a never-before known mechanism of protein control.

"This is the first time we've seen this type of chemical reaction control neuronal differentiation," says Shanthini Sockanathan, Ph.D., an associate professor at the Johns Hopkins Solomon H. Snyder Department of Neuroscience. "And it's probably not specific for motor neurons that we study, but also for development of a wide variety of neurons."

Previous research had shown that the GDE2 protein can cause immature cells in the spinal cord to differentiate into motor neurons, the nerve cells that connect to and control muscle contraction. Too little GDE2 causes motor neurons to not develop, while too much GDE2 causes them to develop too quickly, depleting progenitor pools.

"We reasoned that there must be tight control of GDE2 so we set out to look for the regulator by looking for other proteins that can bind to GDE2," says Sockanathan.

Using biochemical approaches to isolate all proteins that normally bind to GDE2 in the developing spinal cord, followed by proteomic analysis to identify all binding proteins, the research team found a few hundred proteins. One, Prdx1, had been reported by others to have tumor-suppressing abilities, which caught Sockanathan's eye for further investigation.

The team first asked if the Prdx1 protein can affect motor neuron development by removing it from developing spinal cords of chick embryos. Embryos lacking Prdx1 showed loss of motor neurons similar to that seen in embryos lacking GDE2, suggesting that indeed Prdx1 is somehow involved in motor neuron development.

To figure out how Prdx1 and GDE2 interact to cause immature cells to develop into motor neurons, the team mutated the proteins and examined how the mutations affect the cells. Mutations that prevent the two proteins from binding resulted in no motor neurons. Similarly, mutations that disrupt the enzyme abilities of GDE2 and Prdx1 also resulted in no motor neurons. In fact, only when GDE2 and Prdx1 can bind each other and work as enzymes do motor neurons develop.

"So we thought maybe the antioxidant enzyme activity of Prdx1 is doing something to regulate GDE2 function," says Sockanathan. Her team then looked into what already was known about Prdx1's enzyme activity. They found that bacteria and yeast versions of Prdx1 are able to help alter certain chemical bonds in proteins that form between specific amino acids that contain so-called sulfhydryl or "-SH" groups.

That led them to reexamine the GDE2 protein for sulfhydryl groups. As it turns out, they found 4 in GDE2: Three are close together and one is clear on the other end of the protein. They first performed some biochemistry experiments to determine whether these sulfhydryl groups can form disulfide bonds - they can. Then, two at a time, the researchers engineered mutations to replace each -SH-containing amino acid in GDE2 and asked if the mutated protein could still bind to Prx1. They found one combination of mutations that did not behave the same as the unmutated control, leading them to conclude that Prx1 must break the chemical bond between those two specific amino acids.

"We think that Prx1 breaks this bond in GDE2, activating it to promote motor neuron differentiation," says Sockanathan. "This suggests a new general control mechanism that regulates when cells divide and when they differentiate. We're excited to see how widespread it might be."

Découverte de deux gènes qui aident à combattre la sclérose en plaque

ouest-france
01:04 - samedi 12 septembre 2009

Des chercheurs américains ont découvert deux gènes impliqués dans la restauration du système nerveux central de souris atteintes de sclérose en plaque. Cette découverte offre un nouvel espoir pour mettre au point des thérapies plus efficaces et prédire la façon dont les patients répondront à cette maladie auto-immune dégénérative.

L'équipe d'Allan Bieber, spécialiste des neurosciences à la clinique Mayo dans le Minnesota, a étudié des souris atteintes d'une forme chronique de maladie évolutive assimilée à la sclérose en plaque et a cartographié les gènes de celles qui ont spontanément réparé les dommages causés par la maladie. Les chercheurs ont découvert deux facteurs génétiques déterminants dans cette évolution positive

How PCBs May Hurt the Brain

New Studies Shed Light on Exposure to Environmental Toxin and Development of Brain Cells

Kathleen Doheny
WebMD Health News
April 13, 2009

Exposure to environmental toxins known as PCBs have long been linked with behavioral and developmental problems in children, but scientists could never say exactly how PCBs (polychlorinated biphenyls) might adversely affect the brain and lead to the problems.

Now, scientists think they may know.

The chemicals adversely affect the development of brain cells and also make brain circuits "overexcited," which has been linked in previous research to developmental problems, according to researcher Isaac N. Pessah, PhD, a professor of molecular biosciences and director of the University of California Davis Center for Children's Environmental Health.

"We think we have identified the way in which a broad class of environmental contaminants influences the developing nervous system and may contribute to neuro-developmental impairments such as hyperactivity, seizure disorders, and autism," says Pessah, a co-author on a trio of new studies examining the issue. The latest of the three is published online today in PLoS-Biology.

The findings of the three studies are called a "turning point" by another expert in the field.

One surprise finding: low levels of PCB exposure sometimes have greater ill effects than high-dose exposures.

PCBs were widely used for years in many products such as electronic components, pesticides, caulking, and flame retardants, but their production was banned in the U.S. in 1979.

Even so, the chemicals persist in the environment because they don't break down easily, explaining why high levels of PCBs can still be detected in people and in animals. PCBs are found in air, water, soil, and contaminated foods such as fish.

PCB Exposure and Effect on Learning and Brain Cells

In one of the three new studies, exposures to low doses of PCBs in animals hampered their ability to learn to swim a maze, a common test of animal learning.

The low PCB doses also adversely affected the plasticity of the animals' dendrites -- small projections branching out from the neurons or nerve cells that get signals from other cells in the body.

"This plasticity is very important for learning and memory," says study researcher Pamela Lein, PhD, associate professor of neurotoxicology at the UC Davis School of Veterinary Medicine.

The study was published in March in Environmental and Health Perspectives.

Problems in dendrite plasticity and growth have already been implicated in disorders such as autism, schizophrenia, and mental retardation, Lein says.

Lein and colleagues compared the effects of low-dose PCB exposure, high-dose exposure, and no exposure in three groups of rats that had been trained to swim and find an escape platform in a maze, and three groups not trained to swim the maze.

"The PCB treatments did affect the learning and memory," she says. "The effects were seen in the low-dose group but not the high-dose." Those in the low-dose trained group took longer to learn to swim and escape the maze, she says.

In the high-dose group, she says, the exposure may have triggered a compensatory mechanism that protected the brain cells from harm.

PCB Exposure: The Tissue Study

In a second study, the researchers looked at tissue from the animals' hippocampus, an area of the brain that regulates memory and emotion, and measured the "excitability" of neurons there before and during exposures to two different PCBs.

With one of them, says Pessah, "we can get an enhancement of excitability." Normally, information processing in the brain depends on a balance between excitation and inhibition of the neurons.

"Too much excitability is bad for the brain," Pessah says. Many neuro-developmental disorders, he says, including autism and attention deficit hyperactivity disorder or ADHD, "are thought to involve an imbalance between inhibition and excitability."

What they found in this study, he says, is that "even low levels [of PCBs] can tip the balance in the brain." The report is published in March in Toxicology and Applied Pharmacology.

PCB Exposure: The Cellular Level Clues

Finally, the researchers went to the cellular level, trying to find out more specifically how the PCBs change brain cell development as they found in the animal study and how they change the neurons' excitability, as seen in the study on brain tissue.

In the lab, they exposed receptors within the cells that regulate the release of calcium, crucial to maintain normal signaling from cell to cell, to PCBs. When they used electron microscope to create high-resolution images of the interaction between the receptors and the PCBs, they found the chemical binds to the receptors and adversely affects the calcium release. This interference accounts for the findings in the other two studies, Pessah says.

PCB Studies: Second Opinion

"I think that these studies represent a kind of a turning point for our recognition of how these chemicals, PCBs, can interfere with brain development," says R. Thomas Zoeller, PhD, professor of biology at the University of Massachusetts, Amherst. He was a journal reviewer for one study and reviewed the other two for WebMD.

"They are looking at a limited number of forms of PCB chemicals and they are linking exposures to very specific changes in proteins in the nervous system that impact brain development and behavior," he says. Because the animal model studied developmental events that are akin to human developmental events, ''for the first time we are getting a clear view of how these chemicals can impact the brain in humans," he says.

PCB Studies: Practical Applications

The new findings will add weight to the studies finding a link between exposures to PCBs and developmental problems, Lien says. "For the first time, we now have a plausible biological mechanism to explain the effect of PCBs on behavior."

One practical application of the research? Scientists may use the findings to evaluate the safety of numerous chemicals produced to take the place of PCBs, Zoeller says. "Science can't keep up with the rapid kinds of chemical changes that industry can manufacture," he says. "It would be great if we could get out in front of it and identify dangerous chemicals before people are being exposed."

The research findings may also make experts who thought lower-dose PCB exposures were not a problem think again, Pessah says.

'Take control of your sleep, before it takes control of you'

Sify news
Monday, 23 March , 2009, 11:06

New Delhi: If you didn't sleep well last night or feel exhausted all day long, you are probably one of thousands suffering from sleeping disorders. It's possible that hypertension, acidity and several other lifestyle diseases are playing havoc with your sleep.

Good sleep helps you to be alert, awake and keeps you energetic throughout the day and hence a good night's sleep is vital for good health, experts say.

"As sleep is vital to our health and well-being, we must not cut ourselves short from the amount of sleep that we get or suffer from sleep problems. Take control of your sleep problems before it takes control of you," advised Ramnathan Iyer, a doctor who treats patients with sleep disorders.

A good night's sleep boosts immunity

Insomnia refers to the difficulty in initiation, maintenance, duration or quality of sleep. People may experience poor concentration, lower productivity and poorer work quality as a result of insomnia.

Sleep disorders can also make a person fatigued, irritable or forgetful and can lead to strained relationships.

Mumbai-based psychiatrist Manoj Bhatawadekar said: "To prevent or relieve sleep problems and safeguard sleep, making it more restful and pleasurable, it helps to practise good sleep hygiene."

Study links normal sleep and healthy ageing

A good 'sleep hygiene' would entail regular sleep or wake schedule, avoiding naps especially in the evenings, increase exercise, avoid intake of caffeine and alcohol just before sleeping, and schedule reasonable daytime work hours, Bhatawadekar said.

Many experts across the country from the Indian Sleep Disorders Association (ISDA) in association with Abbott India Limited, a health care company, have declared March 3 to April 7 as Sleep Awareness Month to generate awareness about the importance of sleep hygiene.

J C Suri, a doctor and president ISDA, said: "Sleep is important for mental, physical and emotional well-being."

Losing sleep? Blame it on long working hours

Iyer, who is ISDA's west regional governor, stressed: "Early assessment and action can prevent short-term sleep problems from developing into a chronic one."

Hypertension, arthritis, diabetes, acidity and some medications, including some heart medications, may even cause loss of sleep and stress.

When insomnia occurs in the context of chronic illness, it tends to be more severe than other forms of insomnia and usually involves sleep maintenance difficulties. A recent survey revealed that many lifestyle diseases also surfaced as a result of sleep disorders.

Sleep chemical eases brain disorders

Almost two-thirds of those surveyed reported the presence of at least one medical condition. These included 29 percent suffering from hypertension, 28 percent from arthritis, 19 percent coping with heartburn or gastroesophageal reflux disease, 18 percent battling depression, 11 percent dealing with diabetes, 10 percent with heart disease and 5 percent struggling with a lung disease. Obesity also was associated with a greater number of sleep-related problems.

People who reported a medical diagnosis were more likely than people without a diagnosis to sleep less than six hours per night on weekdays and experience symptoms of insomnia, the survey found.