Nintendo Game Console Helps Improve Multiple Sclerosis Rehabilitation

An accessory for the Nintendo Wii game console may help in improving balance and movemenentfor patients with multiple sclerosis.

Researchers published their findings in the journal Radiology. Using Magnetic resonance imaging (MRI) scans, they find that the Nintendo Wii Balance Board system appears to induce favorable changes in brain connections associated with balance and movement.

MS is an autoimmune disease that affects the brain, optic nerve, and spinal cord. In MS, the myelin sheath which is the protective covering that surrounds the nerve cells is attacked by the body's own immune system. The inflamed nerves cause nerve signals to slow down or stop.

The cause of MS is still unknown and there is no known cure for it. Therapies exist that may slow the progression of the disease and treatments focus on controlling the symptoms to help maintain a normal quality of life.

The researches find that the Wii balance board addresses one of the symptoms of MS which is balance impairment. It is one of the most common and disabling symptoms of the disease. The Wii balance board is a battery-powered device about the size and shape of a bathroom scale. Users stand on the board and shift their weight as they follow the action on the television screen during games like slalom skiing.

The image is a 3D rendering showing the starting point (in red, left image), the ending point (in yellow, center image) and the three dimensional rendering (in green, right image) of the nerve tracts examined in the study (Credit: Radiological Society of North America)

Sodium Buildup in Brain Linked To Multiple Sclerosis Disability and Nerve Degeneration

Multiple sclerosis is an autoimmune disease that affects the brain, optic nerve, and spinal cord. The protective covering that surrounds the nerve cells called Myelin Sheaths are damaged which causes nerve signals to slow down or stop.

The damage is caused when the body's own immune system attacks the nervous system causing inflammation. Diseases where the immune system mistakenly attacks normal body cells or tissues are classified as autoimmune diseases.

Multiple sclerosis (MS) affects women more than men and although the disorder can manifest any age, it is commonly diagnosed between ages 20 and 40.

It is still unknown what causes multiple sclerosis but some factors considered are viruses, family history, or a genetic defect.

There is still no known cure for multiple sclerosis although therapies exist that may slow the progression of the disease. MS treatments focuses on controlling the symptoms to help maintain a normal quality of life.

Sodium buildup in brain linked to disability in multiple sclerosis

A buildup of sodium in the brain detected by magnetic resonance imaging (MRI) may be a biomarker for the degeneration of nerve cells that occurs in patients with multiple sclerosis (MS), according to a new study published online in the journal Radiology.

The study found that patients with early-stage MS showed sodium accumulation in specific brain regions, while patients with more advanced disease showed sodium accumulation throughout the whole brain. Sodium buildup in motor areas of the brain correlated directly to the degree of disability seen in the advanced-stage patients.

"A major challenge with multiple sclerosis is providing patients with a prognosis of disease progression," said Patrick Cozzone, Ph.D., director emeritus of the Center for Magnetic Resonance in Biology and Medicine, a joint unit of National Center for Scientific Research (CNRS) and Aix-Marseille University in Marseille, France. "It's very hard to predict the course of the disease."

In MS, the body's immune system attacks the protective sheath (called myelin) that covers nerve cells, or neurons, in the brain and spinal cord. The scarring affects the neurons' ability to conduct signals, causing neurological and physical disability. The type and severity of MS symptoms, as well as the progression of the disease, vary from one patient to another.

Stress Management Program Reduces Multiple Sclerosis Disease Activity

Multiple sclerosis (MS) is an autoimmune disease that affects the brain, optic nerve, and spinal cord. It primarily targets the CNS (central nervous system).

An autoimmune disease is a type of disease where the body's immune system mistakes a normal tissue or cell for a pathogen and attacks it.

MS is caused when the protective covering surrounding nerve cells called myelin sheaths are damaged. When the myelin sheath is damaged, nerve signals travelling through the nerve cells slow down or just stop.

The researchers found that the age-related impairment of the body's ability to replace protective myelin sheaths, which normally surround nerve fibers and allow them to send signals properly, may be reversible, offering new hope that therapeutic strategies aimed at restoring efficient regeneration can be effective in the central nervous system throughout life.

Stress management training may help reduce disease activity in MS

A new study shows that taking part in a stress management program may help people with multiple sclerosis (MS) prevent new disease activity. The study is published in the July 11, 2012, online issue of Neurology®, the medical journal of the American Academy of Neurology.

The study involved 121 people with MS. Half received the stress management program, meeting with a therapist for 16 individual 50-minute sessions over five to six months. They learned about problem-solving skills, relaxation, increasing positive activities, and enhancing their social support. They could also choose optional sessions on topics such as fatigue management, anxiety reduction, pain management and insomnia treatment. After the treatment ended, the participants were followed for another five to six months. The remaining participants were put on a waiting list as a control group. After 10 months, they attended a five-hour workshop on stress management.

Protein Molecule REG3A Lead To New And Better Treatment of Psoriasis

Psoriasis is a chronic inflammatory skin disease.

It is a common skin condition that is not contagious. Psoriasis is identified by dry, red patches of thick skin (called scales) resulting from rapid build up of skin cells. The redness and irritation are usually found around the skin of the elbows, knees, and scalp but can affect any area of the human body.

It is considered an autoimmune disease since the immune system mistakes the skin as a pathogen (infecting agent) and attacks by sending out signals to speed up the growth cycle of skin cells. The difference between psoriasis and other autoimmune disease is that unlike regular autoimmune diseases, there is no presence of any substance that activates the production of antibodies (antigen) to trigger an attack.

Skin cells are replaced about once a month in a process called cell turnover. These cells grow deep in the skin and rises above to replace old skin cells. In psoriasis, because of the signals from the immune system, the process is sped up and is done within days rather than in a month. The dead skin cells then accumulate on the skin surface as newer skin cells are pushed up due to the heightened cell turnover process.

Protein may be key to psoriasis and wound care

Psoriasis is an autoimmune disorder in which skin cells proliferate out of control. For some hard-to-heal wounds, the problem is just the opposite: Restorative skin cells don't grow well or fast enough. In a paper published in the June 21, 2012 issue of Immunity, researchers at the University of California, San Diego School of Medicine describe a molecule that may lead to new treatments for both problems.

An international team of scientists led by principal investigator Richard L. Gallo, MD, PhD, professor of medicine and chief of UC San Diego's Division of Dermatology, analyzed skin biopsies of patients with and without psoriasis, as well as the skin of mice with psoriasis and with wounds on their backs. They discovered that a molecule called regenerating islet-derived protein 3-alpha (REG3A) is highly expressed in skin cells during psoriasis and wound-healing, but not under normal skin conditions.

Discovery May Lead to New Therapy for Autoimmune Diseases

The Immune System protects the body from disease and infection. By design, it attacks and gets rid of sickly and infectious cells that may cause harm to healthy cells around. With an autoimmune disease, the immune system attacks the healthy cells. Autoimmune disease can affect many parts of the body and there are about 80 autoimmune diseases.

Since there are varying symptoms to a specific autoimmune disease, getting diagnosed can be frustrating and stressful. In many people, the first symptoms are being tired, muscle aches and low fever. The diseases may also have flare-ups, when they get worse, and remissions, when they all but disappear. The diseases do not usually go away, but symptoms can be treated.

It is unknown what causes autoimmune diseases but research suggests that in many cases, it is an inherited predisposition (such as Type 1 Diabetes). With rheumatic fever and other types of autoimmune disease, a virus or infection with bacteria triggers an immune response and the antibodies or T-cells attack normal cells because some part of their structure resembles a part of the infecting microorganism.

Autoimmune disorders fall into two general types: those that damage many organs (systemic autoimmune diseases) and those where only a single organ or tissue is directly damaged by the autoimmune process (localized). However, the distinctions become blurred as the effect of localized autoimmune disorders frequently extends beyond the targeted tissues, indirectly affecting other body organs and systems.

Autoimmune diseases, such as Type I diabetes and rheumatoid arthritis, are caused by an immune system gone haywire, where the body's defense system assaults and destroys healthy tissues. A mutant form of a protein called LYP has been implicated in multiple autoimmune diseases, but the precise molecular pathway involved has been unknown. Now, in a paper in Nature Chemical Biology, researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) show how the errant form of LYP can disrupt the immune system. In doing so, they also found a potential new therapy for autoimmune diseases—a chemical compound that appears to inhibit this mutant protein.