The World Health Organization has projected that by 2020, major depression will be the second-most significant cause for disability in the world, after heart disease. Along with psychotherapy, the disorder is usually treated using antidepressant drugs. There is often a frustrating trial-and-error period involved in finding the right drug for the right person, however, while side effects can include obesity, sexual dysfunction, and fatigue … to name a few. Los Angeles-based company NeuroSigma is now looking into an alternative drug-free therapy, that could ultimately incorporate electrodes implanted under the patient’s skin.

In an eight-week clinical trial conducted last June, researchers at UCLA externally stimulated the cranial trigeminal nerve of patients who suffered from depression. This was accomplished by attaching two electrodes to the skin of each subject’s forehead, which were in turn attached to a mobile phone-sized stimulating device. The external Trigeminal Nerve Stimulation (eTNS) process reportedly resulted in a 70 percent reduction in symptom severity during the trial, and a subsequent 80 percent remission rate, with none of the side effects associated with antidepressants.

The technology is licensed exclusively to NeuroSigma.

Last month, findings were presented on four more subjects from those trials, including functional neuroimaging PET data. It was determined that even brief exposure to eTNS increased blood flow to regions of the brain associated with depression and mood regulation. “These findings of a potential mechanism of action support our original hypothesis that electrical stimulation of the trigeminal nerves, located in facial skin tissue, can provide a very safe and effective means to send signals to key structures deep in the brain, thus providing a high-bandwidth pathway to the brain without current penetrating directly through the skull” said UCLA‘s Dr. Ian Cook.

A twenty-subject, double-blind second phase of the trials began this February, and should wrap up late this year.

NeuroSigma is meanwhile continuing development of eTNS, while also working on a version of the system that would utilize implantable subcutaneous electrodes. Known as sTNS, patients who responded well to eTNS could choose to switch over to it. The technology could also possibly be used to treat epilepsy and post-traumatic stress disorder.

Sourced & published by Henry Sapiecha

BRAIN LOSING CONSCIOUSNOUS CAN BE TRACKED

Using a newly developed imaging technique, researchers in the U.K. have for the first time observed what happens to the brain as it loses consciousness. The method known as “functional electrical impedance tomography by evoked response” (fEITER) uses a 32 electrode array to scan the brain at a rate of 100 times a second and by applying this as an anaesthetic drug takes effect, researchers are able to build a real-time 3-D video that will aid in better understanding of how the brain functions and the nature of consciousness.

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The multidisciplinary team from the University of Manchester are the first to apply electrical impedance tomography (EIT) to anaesthesia.

So far the evidence supports the theory put forward by Oxford University’s Professor Susan Greenfield that consciousness is not an ON/OFF state but more like a dimmer switch.

“Our findings suggest that unconsciousness may be the increase of inhibitory assemblies across the brain’s cortex,” said Brian Pollard, Professor of Anaesthesia at The University of Manchester (UK). “These findings lend support to Greenfield’s hypothesis of neural assemblies forming consciousness.

“We have looked at 20 healthy volunteers and are now looking at 20 anaesthetized patients scheduled for surgery. We are able to see 3-D images of the brain’s conductivity change, and those where the patient is becoming anaesthetized are most interesting.”

“We have been able to see a real time loss of consciousness in anatomically distinct regions of the brain for the first time. We are currently working on trying to interpret the changes that we have observed. We still do not know exactly what happens within the brain as unconsciousness occurs, but this is another step in the direction of understanding the brain and its functions.”

EIT also holds promise in diagnosing changes to the brain that occur as a result of head injury, stroke and dementia.

“If its power can be harnessed, then it has the potential to make a huge impact on many areas of imaging in medicine,” said Pollard.

The findings are were presented earlier this month at the European Anaesthesiology Congress in Amsterdam.

Source: University of Manchester.

Sourced & Published by Henry Sapiecha

Head-worn device uses sonar to rapidly diagnose stroke
A team of radiologists and retired US Navy sonar experts have used technology developed for submarines as the basis for a new device which offers quick detection, diagnosis and monitoring of stroke. Combined with a portable laptop based console, the head-worn device enables different types of stroke and brain injury to be discovered and located, differentiating normal blood flow from life threatening conditions and delivering an initial diagnosis in under a couple of minutes. Read More

Received & published by Henry Sapiecha

The 7-minute exercise plan for diabetes prevention

Exercise is overrated. I’m always reading more proof that says you don’t need to run a marathon to receive the benefits of a little exercise. Like this British study that claims you can control or prevent diabetes with as little as seven minutes of exercise… per week.

The study’s leader, University of Edinburgh biologist James Timmons, says that you can get the same benefits from minimal amounts of exercise as you can from workouts that last for hours. “This is such a brief amount of exercise you can do it without breaking a sweat,” Timmons said.

In the study, out-of-shape men in their 20s were asked to ride an exercise bike a few times each day – in 30 second bursts of pedaling – two days a week. After just two weeks, the all of the men were 23 % more effective at processing the insulin.

I’ve warned you many times about the potential dangers of over-rigorous exercise, so this minimalist approach appeals to me – and it should to you, too! Like I always say, skip the gym membership and just go for a brisk walk.

Always providing your brain with vigorous exercise,

William Campbell Douglass II, M.D.

Sourced & published by Henry Sapiecha

Deathstalker Scorpion Venom

Could Improve Gene Therapy

for Brain Cancer

Science (Aug. 11, 2010) — An ingredient in the venom of the “deathstalker” scorpion could help gene therapy become an effective treatment for brain cancer, scientists are reporting. The substance allows therapeutic genes — genes that treat disease — to reach more brain cancer cells than current approaches, according to the study in ACS Nano.

Miqin Zhang and colleagues note that gene therapy — the delivery of therapeutic genes into diseased cells — shows promise for fighting glioma, the most common and most serious form of brain cancer. But difficulties in getting genes to enter cancer cells and concerns over the safety and potential side effects of substances used to transport these genes have kept the approach from helping patients.

The scientists describe a new approach that could solve these problems. Key ingredients of their gene-delivery system are chlorotoxin, the substance in deathstalker scorpion venom that can slow the spread of brain cancer, and nanoparticles of iron oxide. Each nanoparticle is about 1/50,000th the width of a human hair. In tests on lab mice, the scientists demonstrated that their venom-based nanoparticles can induce nearly twice the amount of gene expression in brain cancer cells as nanoparticles that do not contain the venom ingredient. “These results indicate that this targeted gene delivery system may potentially improve treatment outcome of gene therapy for glioma and other deadly cancers,” the article notes.

Sourced & published by Henry Sapiecha

New ‘hand’ may alleviate phantom pain

JENA, Germany (UPI) — Amputees suffering from “phantom pain” may get relief from a modified prosthetic that can convince the brain the body part still exists, researchers say.

Scientists at the University of Jena in Germany say phantom pain often lasts for years, and sometimes for a lifetime, often putting amputees at risk of mediation addiction from high dosages of painkillers, a university release said Friday.

Researchers say they’ve produced a modified prosthetic hand than can reduce phantom pain following amputation by using a stimulation unit in the hand’s cuff connected to the remaining part of the upper arm.

Modern prosthetic hands have pressure sensors meant to regulate the strength of grip of the artificial hand depending on what the wearer is trying to pick up, such as a raw egg or a hammer.

The stimulation unit in the modified hand takes feedback from the sensors and “talks” to the wearer’s brain, Dr. Gunther Hofmann of the Jena Department for Trauma, Hand and Reconstructive Surgery says.

“Our system is now able to transmit this sensory information from the hand to the upper arm,” Hofmann says.

Brain structures responsible for processing sensory information coming from the lost body part are “out of work” following an amputation and try to reorganize themselves, often leading to sensations of pain in a “phantom” hand, the Jena researchers say. By giving the appropriate brain structure sensory input from the “hand” it is meant to control, the reorganization can be prevented or reversed, thus eliminated phantom pain, they say.

Copyright 2010 by United Press International

Sourced & published by Henry Sapiecha

Study: Music training ‘primes’ the brain

EVANSTON, Ill. (UPI) — Musical instruction can “prime” the brain to improve human skills in language, speech, memory and attention, U.S. researchers say.

A study at Northwestern University found the effects of musical training on the nervous system can build meaningful patterns important to all types of learning, ScienceDaily.com reported Tuesday.

Researchers studied music training’s effect on neuroplasticity, defined as the brain’s ability to adapt and change as a result of training and experience over the course of a person’s life.

An active engagement with musical sounds not only enhances neuroplasticity, Nina Kraus, director of Northwestern’s Auditory Neuroscience Laboratory, said, but also creates permanent patterns important to all learning.

“The brain is unable to process all of the available sensory information from second to second, and thus must selectively enhance what is relevant,” Kraus said.

“A musician’s brain selectively enhances information-bearing elements in sound,” Kraus said, and “the nervous system makes associations between complex sounds and what they mean.”

These efficient sound-to-meaning connections are important not only for music but for other aspects of communication, she said.

“The effect of music training suggests that, akin to physical exercise and its impact on body fitness, music is a resource that tones the brain for auditory fitness,” the study said.

Copyright 2010 by United Press International

Sourced & published by Henry Sapiecha

Protein could battle Alzheimer’s disease

NEW YORK (UPI) — U.S. researchers say they are looking at a new approach to treating Alzheimer’s disease with a protein thought to extend lifespan in laboratory animals.

Scientists at the Massachusetts Institute of Technology said that in mice prone to developing Alzheimer’s, activating a protein called sirtuin suppressed the disease and destroying the protein made the disease much worse, The New York Times reported.

The finding raises the hope that Alzheimer’s, and possibly other neurodegenerative diseases like Parkinson’s and Huntington’s, could be treated with drugs that activate sirtuin, researchers say.

“We think it is a scientifically compelling story that ties the sirtuins to the biology of Alzheimer’s disease,” said Dr. Dennis J. Selkoe, an Alzheimer’s expert at Harvard Medical School who was not a part of the study.

Drugs that activate sirtuin already exist, including resveratrol, a minor ingredient of red wine and other foods.

One drug company, Sirtris, is in preclinical trials with sirtuin-activating drugs.

“We think it has very significant potential in neurodegenerative diseases,” Sirtris Chief Executive Officer George P. Vlasuk said.

Copyright 2010 by United Press International

Sourced & published by Henry Sapiecha

Of Bugs and Brains:

Gut Bacteria Affect Multiple Sclerosis

Science (July 20, 2010) — Biologists at the California Institute of Technology (Caltech) have demonstrated a connection between multiple sclerosis (MS) — an autoimmune disorder that affects the brain and spinal cord — and gut bacteria.

The work — led by Sarkis K. Mazmanian, an assistant professor of biology at Caltech, and postdoctoral scholar Yun Kyung Lee — appears online the week of July 19-23 in the Proceedings of the National Academy of Sciences.

Multiple sclerosis results from the progressive deterioration of the protective fatty myelin sheath surrounding nerve cells. The loss of myelin hinders nerve cells from communicating with one another, leading to a host of neurological symptoms including loss of sensation, muscle spasms and weakness, fatigue, and pain. Multiple sclerosis is estimated to affect about half a million people in the United States alone, with rates of diagnosis rapidly increasing. There is currently no cure for MS.

Although the cause of MS is unknown, microorganisms seem to play some sort of role. “In the literature from clinical studies, there are papers showing that microbes affect MS,” Mazmanian says. “For example, the disease gets worse after viral infections, and bacterial infections cause an increase in MS symptoms.”

On the other hand, he concedes, “it seems counterintuitive that a microbe would be involved in a disease of the central nervous system, because these are sterile tissues.”

And yet, as Mazmanian found when he began examining the multiple sclerosis literature, the suggestion of a link between bacteria and the disease is more than anecdotal. Notably, back in 1993, Caltech biochemist Leroy Hood — who was then at the University of Washington — published a paper describing a genetically engineered strain of mouse that developed a lab-induced form of multiple sclerosis known as experimental autoimmune encephalomyelitis, or EAE.

When Hood’s animals were housed at Caltech, they developed the disease. But, oddly, when the mice were shipped to a cleaner biotech facility — where their resident gut bacterial populations were reduced — they didn’t get sick. The question was, why? At the time, Mazmanian says, “the authors speculated that some environmental component was modulating MS in these animals.” Just what that environmental component was, however, remained a mystery for almost two decades.

But Mazmanian — whose laboratory examines the relationships between gut microbes, both harmful and helpful, and the immune systems of their mammalian hosts — had a hunch that intestinal bacteria were the key. “As we gained an appreciation for how profoundly the gut microbiota can affect the immune system, we decided to ask if symbiotic bacteria are the missing variable in these mice with MS,” he says.

To find out, Mazmanian and his colleagues tried to induce MS in animals that were completely devoid of the microbes that normally inhabit the digestive system. “Lo and behold, these sterile animals did not get sick,” he says.

Then the researchers decided to see what would happen if bacteria were reintroduced to the germ-free mice. But not just any bacteria. They inoculated mice with one specific organism, an unculturable bug from a group known as segmented filamentous bacteria. In prior studies, these bacteria had been shown to lead to intestinal inflammation and, more intriguingly, to induce in the gut the appearance of a particular immune-system cell known as Th17. Th17 cells are a type of T helper cell — cells that help activate and direct other immune system cells. Furthermore, Th17 cells induce the inflammatory cascade that leads to multiple sclerosis in animals.

“The question was, if this organism is inducing Th17 cells in the gut, will it be able to do so in the brain and central nervous system?” Mazmanian says. “Furthermore, with that one organism, can we restore to sterile animals the entire inflammatory response normally seen in animals with hundreds of species of gut bacteria?”

The answer? Yes on all counts. Giving the formerly germ-free mice a dose of one species of segmented filamentous bacteria induced Th17 not only in the gut but in the central nervous system and brain — and caused the formerly healthy mice to become ill with MS-like symptoms.

“It definitely shows that gut microbes have a strong role in MS, because the genetics of the animals were the same. In fact, everything was the same except for the presence of those otherwise benign bacteria, which are clearly playing a role in shaping the immune system,” Mazmanian says. “This study shows for the first time that specific intestinal bacteria have a significant role in affecting the nervous system during MS — and they do so from the gut, an anatomical location very, very far from the brain.”

Mazmanian and his colleagues don’t, however, suggest that gut bacteria are the direct cause of multiple sclerosis, which is known to be genetically linked. Rather, the bacteria may be helping to shape the immune system’s inflammatory response, thus creating conditions that could allow the disease to develop. Indeed, multiple sclerosis also has a strong environmental component; identical twins, who possess the same genome and share all of their genes, only have a 25 percent chance of sharing the disease. “We would like to suggest that gut bacteria may be the missing environmental component,” he says.

For their part, Th17 cells are needed for the immune system to properly combat infection. Problems only arise when the cells are activated in the absence of infection — just as disease can arise, Mazmanian and others suspect, when the species composition of gut bacteria become imbalanced, say, by changes in diet, because of improved hygiene (which kills off the beneficial bacteria as well as the dangerous ones), or because of stress or antibiotic use. One impact of the dysregulation of normal gut bacterial populations — a phenomenon dubbed “dysbiosis” — may be the rising rate of multiple sclerosis seen in recent years in more hygienic societies.

“As we live cleaner, we’re not just changing our exposure to infectious agents, but we’re changing our relationship with the entire microbial world, both around and inside us, and we may be altering the balance between pro- and anti-inflammatory bacteria,” leading to diseases like MS, Mazmanian says. “Perhaps treatments for diseases such as multiple sclerosis may someday include probiotic bacteria that can restore normal immune function in the gut… and the brain.”

The work was supported by funding from the California Institute of Technology, the Weston Havens Foundation, and the Edward Mallinckrodt, Jr. Foundation.

Sourced & published by Henry Sapiecha

Alzheimers  treatment with Curcumin in CURRY

Cooking with Curry: How Curcumin Can Prevent Alzheimer’s Disease

Curcumin is a powerful antioxidant that is found in curry powder and used in traditional Indian cooking. The blending of curcumin with other spices has made this seasoning appeal more to the European pallet and has made the ingredient a popular and healthy choice for seasoning many different dishes. However, more than just your taste buds will benefit from curry. Curry, and more specifically curcumin, has been found to help prevent Alzheimer’s disease.

The preventative quality of curry goes beyond its basic antioxidant function. Curcumin has been found effective in slowing or stopping the formation of protein fragments in brain cells. It is able to do this so effectively because it has such a low molecular weight. This enables it to seep into the blood stream better and bind to the beta amyloid plaque that forms on the brains of Alzheimer’s patients. So curry is good at not only preventing Alzheimer’s disease, but it removing some plaques of those already in the early stages.

If you don’t think that curry can do all that it claims, consider the fact that adults between the ages of 70-79 in India had a four times lower rate of Alzheimer’s disease in one 2003 study. The conclusion that researcher drew is that the difference is in the curry. The yellow, powdery food preservative, curcumin, found in curry, is found in abundance in the traditional Indian diet.

Here are some great uses for curry that will spice up your diet and put this strong antioxidant to work in cleaning up brain plaque that may already be forming. Curry can be a very strong flavor that some people just don’t like. For those who don’t care for it, the flavor can be played down as in the following recipes, keeping all of the nutritional benefits in.

1. Sprinkle some curry powder on your chicken salad. Adding halved red grapes and green onions balances the strength of the curry flavor. It’s also great with toasted almond slivers. You can serve it on a bed of dark green spinach or in half a tomato to add to the nutritional value.
2. Vitamins A and C are abundant in a traditional Bombay rice dish that has both curry powder and cumin. Use brown rice as your base adding chick peas, apricots, zucchini, onion, and any other vegetables you like such as carrots and red pepper. This can be cooked in a vegetable or fat-free chicken broth until the rice is cooked through. Just a tablespoon of curry powder and a teaspoon of cumin to 1 ½ cups uncooked rice balances the recipe.
3. Try adding 1/8 teaspoon of curry powder to low-fat or fat-free mayonnaise to spice up your next turkey sandwich. Load on the fresh lettuce, raw spinach, tomatoes, and peppers and put the balanced meal into a whole-wheat pita pocket.
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   Curry can be added subtly into many different recipes eliminating the need for salt. Check to be sure that your curry seasoning does not have added salt, or use just plain cumin in its place. You’ll spice up your meals while protecting your brain.

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Learn how to maintain good mental health at: http://www.alzheimersdefense.com/

Sourced and published by Henry Sapiecha 17th March 2010