Swedish discovery could lead to new stroke therapy

ScienceDaily (Feb. 18, 2011) — The opportunities to treat a stroke have long been limited to the hours after an attack. The loss of brain function caused by the stroke has previously been regarded as permanent. Brain researchers at Lund University have now discovered a substance that opens up the possibility of treatment up to two days after a stroke.

See Also:Health & MedicineStroke PreventionElder CareHeart DiseaseMind & BrainBrain InjuryStrokeCaregivingReferenceMulti-infarct dementiaBrain damagePeripheral visionStroke

The only acute treatment for a stroke currently available is thrombolysis. This uses drugs that dissolve the blood clot responsible for the stroke, but it only reaches around 10 per cent of stroke patients in time to prevent lasting damage. For other patients, there are no other effective drugs that reduce the loss of brain function following a stroke.

Researchers at the Laboratory for Experimental Brain Research in Lund, together with American researchers, have discovered a substance that reinforces the brain's self-healing functions after a stroke. It has long been known that people affected by a stroke can regain some lost function during the first six months. Professor Tadeusz Wieloch and his colleagues have found a way to activate a protein in the brain, the sigma-1 receptor, which plays an important role in the brain's recovery during the critical period after the injury.

The study, which is published in the scientific journal Brain, began with experiments on rats. The animals were subjected to a stroke and then placed in different environments -- an enriched cage with extra stimulation in the form of several levels of tubes, beams and ladders, and a normal cage.

"After performing a genetic analysis of the rats that stayed in the normal cage and those that were in an enriched cage, we found that many genes were activated by the enriched environment. One of these genes coded for the protein sigma-1 receptor. We then injected the rats with a specific substance that activated the sigma-1 receptor and found that the rats regained their function more quickly than the untreated animals," explains Professor Wieloch.

The idea is to recreate and reinforce the brain's natural response to an enriched environment. By injecting the activating substance, brain repair is stimulated. This result of Swedish basic research, which started over 15 years ago, has led to a clinical trial on stroke patients by a Japanese pharmaceutical company.

"We are very pleased that our research on stroke here in Lund has made it all the way from our experiments in the lab to an international clinical trial," says Professor Wieloch.

"This is an excellent example of how basic research can be translated into a healthcare setting and possibly lead to new and better therapies. It also exemplifies the fact that, within medical research, it is a long journey from experimental studies to results that benefit the patient," says Professor Wieloch.

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Device measures brain temperature non-invasively: Monitoring could be critical in life-saving cooling therapy

ScienceDaily (May 3, 2011) — Doctors have long sought a way to directly measure the brain's temperature without inserting a probe through the skull. Now researchers have developed a way to get the brain's precise temperature with a device the diameter of a poker-chip that rests on a patient's head, according to findings presented May 1 at the annual meeting of the Pediatric Academic Societies in Denver.

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"This is the first time that anyone has presented data on the brain temperature of a human obtained non-invasively," said principal researcher Dr, Thomas Bass, a neonatologist at Children's Hospital of The King's Daughters in Norfolk, Va., and a professor of pediatrics at the hospital's academic partner, Eastern Virginia Medical School.

The research also suggests that an injured brain can be significantly warmer than the body, a finding critical to cooling therapies that reduce brain damage in everyone from elderly heart attack victims to hypoxic newborns.

"Knowing the actual brain temperature may allow us to improve outcomes by keeping the brain at an optimum temperature," said Dr. Bass.

With the help of a $750,000 National Institutes of Health grant, a research team led by Dr. Bass adapted an instrument that calculates temperatures by detecting microwave emissions produced by all human tissue.

Those microwaves pass unimpeded through the skull, like light passing through a sheet of glass. As tissue temperatures increase, the emissions grow more intense. Engineers calibrated the device to measure the temperature of brain tissue 1.5 centimeters beneath the skull.

In the trial whose results were presented, the device was placed on the heads of infants undergoing cooling therapy at CHKD. The device's brain temperature readings were correlated with rectal and esophageal temperatures. The difference in temperature between the brain and the body recorded by other means was as high as 5.4% Fahrenheit.

"That's difference is larger than we expected," Dr. Bass said.

Dr. Bass, who pioneered research on cooling therapy for hypoxic newborns, and set about this research because he believed the therapy could be improved if doctors knew precise temperature of the damaged organ, the brain.

Hypoxic brain damage in infants occurs most often in full-term births when the child suffers oxygen loss either immediately before or during delivery. Because of a quirk in the brain, a child can be revived but brain cells continue to die over several days, resulting in brain damage or death. Doctors could do little to stop this progression; parents often watched helplessly as their sons and daughters literally died before their eyes.

Based on the observation that children rescued from freezing ponds after extended periods of time suffered little or no brain damage, cooling therapy involves chilling an infant's body to 92 degrees for 72 hours after brain injury.

A clinical trial on the therapy showed that cooling the child stops or reduces the progression of brain cell death, drastically reducing brain damage and death. The results were so positive that the therapy is now standard in advanced neonatal intensive-care units worldwide.

Cooling therapy is now used with other patients as well, including heart attack victims whose brains have suffered oxygen deprivation.

Because cooling therapy's success relies on the temperature of the brain, precise readings of the brain's temperature is likely to improve a therapy that's already proven remarkably effective.

Children's Hospital of The King's Daughters is the only freestanding pediatric hospital in Virginia.

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Viagra could reduce multiple sclerosis symptoms, study suggests

ScienceDaily (May 19, 2011) — Universitat Autònoma de Barcelona researchers have discovered that Viagra®  (sildenafil) drastically reduces multiple sclerosis symptoms in animal models with the disease. The research, published in Acta Neuropathologica, demonstrates that a practically complete recovery occurs in 50% of the animals after eight days of treatment. Researchers are confident that clinical trials soon will be carried out in patients given that the drug is well tolerated and has been used to treat sexual dysfunction in some multiple sclerosis patients.

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Multiple sclerosis is the most common chronic inflammatory disease of the central nervous system and one of the main causes of disability among young adults. The disease is caused by the presence of multiple focuses of demyelination (loss of myelin sheaths around the axons, affecting the ability of neurons to communicate) and neurodegeneration in different areas of the central nervous system. There is currently no cure for the disease, although some drugs have proven effective in fighting symptoms and preventing it from progressing.

A research team from the UAB Institute of Biotechnology and Biomedicine directed by Dr Agustina García, in collaboration with the research team directed by Dr Juan Hidalgo from the UAB Institute of Neurosciences, has studied the effects of a treatment using sildenafil, sold as Viagra®, in an animal model of multiple sclerosis known as experimental autoimmune encephalomyelitis (EAE). Researchers demonstrated that a daily treatment with sildenafil after disease onset quickly reduced clinical signs, with a practically complete recovery in 50% of the cases after eight days of treatment. Scientists observed how the drug reduced the infiltration of inflammatory cells into the white matter of the spinal cord, thus reducing damage to the nerve cell's axon and facilitating myelin repair.

Sidenafil, together with tadalafil (Cialis®) and vardenafil (Levitra®), form part of a group of vasodilator drugs known as phosphodiesterase type 5 (PDE5) inhibitors, used in the treatment of erectile dysfunction and pulmonary arterial hypertension. Recent studies in animal models of central nervous system pathologies already pointed to the fact that in addition to vasodilation, these drugs could contain other neuroprotective actions and suggest their usefulness as possible treatments of both acute (cerebrovascular stroke) and chronic (Alzheimer's) neuropathologies.  Research published in 2010 in the Journal of Neurochemistry by the same research group from UAB demonstrated that one of these inhibitors reduced neuroinflammation and neuronal damage in animal models of traumatic brain injury.

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