Showing posts with label stroke. Show all posts
Showing posts with label stroke. Show all posts

Wednesday, June 1, 2011

Culprit found for increased stroke injury with diabetes

ScienceDaily (Jan. 24, 2011) — Strokes are a leading cause of mortality and adult disability. Those that involve intracerebral hemorrhage (bleeding in the brain) are especially deadly, and there are no effective treatments to control such bleeding. Moreover, diabetes and hyperglycemia (high blood glucose levels) are associated with increases in bleeding during hemorrhagic stroke and worse clinical outcomes.

See Also:Health & MedicineDiabetesHeart DiseaseDiseases and ConditionsMind & BrainBrain InjuryStrokeDisorders and SyndromesReferenceHyperglycemiaBlood sugarDiabetes mellitus type 2Glycemic index

But Joslin Diabetes Center researchers now have identified one key player that contributes to this increased bleeding, a discovery that may pave the way toward treatments that minimize adverse stroke outcomes both for people with pre-existing diabetes and those with hyperglycemia identified at the time of stroke.

Studies in the lab of Joslin Investigator Edward Feener, Ph.D., pinpointed a new mechanism involving a protein called plasma kallikrein that interferes with the normal clotting process in the brain following blood vessel injury with diabetes. Their work is reported online in the journal Nature Medicine.

The scientists began by injecting a small amount of blood into the brains of rats with diabetes and of control animals without diabetes. The difference was dramatic -- the diabetic animals bled over a much greater area of the brain.

Work in the Feener lab had previously implicated plasma kallikrein in diabetic eye complications. When the experimenters pre-treated the diabetic animals with a molecule that inhibits the protein's effects, brain damage from the blood injections dropped to levels similar to that in the control animals. Conversely, when pure plasma kallikrein was injected into the brain, it produced little impact on the control animals but rapidly increased major bleeding in the animals with diabetes.

Further studies by the Joslin researchers showed that normalizing blood glucose levels in diabetic animals could block the effect from plasma kallikrein, and that rapidly inducing hyperglycemia in control animals mimicked the effects of diabetes on brain hemorrhage. This suggests that high blood sugar at the time of brain hemorrhage, rather than diabetes per se, is responsible for the increased bleeding.

"Given the prevalence of strokes and the damage they inflict, these findings are exciting because they suggest the possibility that rapid control of blood sugar levels may provide an opportunity to reduce intracerebral hemorrhage, which is a clinical situation that has very limited treatment options," says Dr. Feener, who is also an associate professor of medicine at Harvard Medical School. "This work could have broad implications since about half of patients with acute hemorrhagic stroke have hyperglycemia, whether or not they have pre-existing diabetes."

The work also raises the possibility of developing drugs that target plasma kallikrein and may provide protective measures in people with diabetes or others at high risk for stroke. Such drugs might also prove useful for patients suffering from the more common ischemic strokes, which usually begin as blocked vessels in the brain but can transform into hemorrhages.

Surprisingly, while plasma kallikrein has been studied for decades, the Joslin scientists found that the protein boosts brain bleeding through a previously unknown mechanism -- by blocking platelet activation near damaged blood vessels.

Joslin's Jia Liu and Ben-Bo Gao were co-lead authors on the Nature Medicine paper. Other contributors include Joslin's Allen Clermont, and Price Blair and Robert Flaumenhaft of Beth Israel Deaconess Medical Center, and Tamie Chilcote and Sukanto Sinha of ActiveSite Pharmaceuticals. Lead funding came from the National Institutes of Health and the American Heart Association.

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Tuesday, May 31, 2011

The changing roles of two hemispheres in stroke recovery

ScienceDaily (Jan. 31, 2011) — Most people who survive a stroke recover some degree of their motor, sensory and cognitive functions over the following months and years. This recovery is commonly believed to reflect a reorganisation of the central nervous system that occurs after brain damage. Now a new study, published in the February 2011 issue of Elsevier's Cortex, sheds further light on the recovery process through its effect on language skills.

See Also:Health & MedicinePsychology ResearchNervous SystemBrain TumorMind & BrainBrain InjuryIntelligenceLanguage AcquisitionReferenceBrain damageThalamusAmnesiaFunctional neuroimaging

For almost all right-handed people and for about 60% of left-handers, damage to the left side of the brain causes a condition known as aphasia, an acute or chronic impairment of language skills. The syndrome is strongly associated with damage to the left hemisphere of the brain; however, there is a long-standing controversy regarding the involvement of parts of the right hemisphere in language functions and their contribution to recovery from aphasia. The majority of experts stress the role of the dominant left side in language recovery, while others argue for a complementary (or compensatory) function of the right hemisphere.

Odelia Elkana, from the Hebrew University, Jerusalem, and colleagues investigated the systematic patterns of reorganisation in the brain's language functions, and their relation to linguistic performance, in patients recovering from childhood brain damage to the left hemisphere. They used functional MRI to detect patterns of brain activity while patients performed various linguistic tasks inside the scanner. The new study focused on a rare group of children whose brain damage had occurred after they had already developed language skills but while the brain was still developing, and therefore most able to reorganise its language functions.

According to the authors, the findings suggest that "recovery is a dynamic, ongoing process, may last for years after onset and is reflected in an increasing proficiency of inter-hemispheric coordination, rather than just in an increase of activation in one side or the other. Therefore, the role of each hemisphere in the recovery process is not only dependent on the stage of recovery (acute, sub-acute or chronic stage), but also within each of these stages it may continuously change over time."

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Hope for stroke victims

ScienceDaily (Feb. 8, 2011) — Much of the devastation of stroke and head trauma is due to damage caused the overproduction of a substance in the brain called glutamate. Preventing this damage has been impossible, until now, as many drugs don't cross the so-called blood-brain barrier, and those that do often don't work as intended. But a method originally devised at the Weizmann Institute of Science may, in the future, offer a way to avert such glutamate-induced harm.

See Also:Health & MedicineBrain TumorStroke PreventionPsychology ResearchMind & BrainBrain InjuryDisorders and SyndromesMultiple SclerosisReferenceAstrocyteExcitotoxicity and cell damageDopamine hypothesis of schizophreniaGlutamic acid

Prof. Vivian I. Teichberg of the Institute's Neurobiology Department first demonstrated a possible way around these problems in 2003. Glutamate -- a short-lived neurotransmitter -- is normally all but absent in brain fluids. After a stroke or injury, however, the glutamate levels in brain fluid become a flood that over-excites the cells in its path and kills them. Instead of attempting to get drugs into the brain, Teichberg had the idea that one might be able to transport glutamate from the brain to the blood using the tiny "pumps," or transporters, on the capillaries that work on differences in glutamate concentration between the two sides. Decreasing glutamate levels in blood would create a stronger impetus to pump the substance out of the brain. He thought that a naturally-occurring enzyme called glutamate-oxaloacetate transaminase (GOT, for short) could "scavenge" blood glutamate, significantly lowering its levels. By 2007, Teichberg and his colleagues had provided clear evidence of the very strong brain neuroprotection that oxolacetate (a chemical similar to GOT) afforded rats exposed to a head trauma.

Two new studies -- conducted by Francisco Campos and others from the lab of Prof. Jose Castillo in the University of Santiago de Compostela, Spain -- now provide a definitive demonstration of Teichberg's results. In the first, the scientists conclusively showed that oxoloacetate injected into rats with stroke-like brain injuries reduces glutamate levels both in the blood and in the affected brain region, while significantly lessening both cell death and the swelling that can accompany stroke. In the second, a team of neurologists in two different hospitals checked the levels of glutamate and GOT in several hundred stroke victims who were admitted to their hospitals. They found that the most significant predictor of the prognosis -- how well they would recover at three months and how much brain damage they would suffer -- was the levels of these two substances. High glutamate levels correlated with a poor outcome, high GOT levels with a better one.

The overall implication of these two papers is that administering GOT might improve a patient's chances of recovering, as well as speeding up the process. In addition to stroke and head trauma, a number of diseases are characterized by an accumulation of glutamate in the brain, including Alzheimer's disease, Parkinson, multiple sclerosis, epilepsy, glaucoma, certain brain tumors and amyotrophic lateral sclerosis, and there is hope that, in the future, treatments to scavenge glutamate could relieve the symptoms and improve the outcomes for a number of neurological problems. Yeda, the technology transfer arm of the Weizmann Institute, holds a patent for this method.

Prof. Vivian I. Teichberg's research is supported by the Nella and Leon Benoziyo Center for Neurosciences; the Carl and Micaela Einhorn-Dominic Brain Research Institute; and the Legacy Heritage Fund Program of the Israel Science Foundation. Prof. Teichberg is the incumbent of the Louis and Florence Katz-Cohen Professorial Chair of Neuropharmacology.

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Monday, May 30, 2011

Advanced macular degeneration is associated with an increased risk of bleeding stroke, study finds

ScienceDaily (Feb. 10, 2011) — Older people with late-stage, age-related macular degeneration (AMD) appear to be at increased risk of brain hemorrhage (bleeding stroke), but not stroke caused by brain infarction (blood clot), according to research presented at the American Stroke Association's International Stroke Conference 2011.

See Also:Health & MedicineStroke PreventionElder CareBrain TumorMind & BrainBrain InjuryStrokeDisorders and SyndromesReferencePeripheral visionMulti-infarct dementiaCerebral contusionBrain damage

"Other studies have found there are more strokes in older individuals with late AMD, but ours is the first to look at the specific types of strokes," said Renske G. Wieberdink, M.D., study researcher and epidemiologist at Erasmus Medical Center in Rotterdam, the Netherlands. "We found the association is with brain hemorrhage, but not brain infarction."

AMD is degeneration of the macula, which is the part of the retina responsible for the sharp, central vision needed to read or drive. Because the macula primarily is affected in AMD, central vision loss may occur. Age-related macular degeneration usually produces a slow, painless loss of vision. Early signs of vision loss from AMD include shadowy areas in your central vision or unusually fuzzy or distorted vision.

Because the number of brain hemorrhages observed in the study was small, the findings will need to be corroborated in a larger group, Wieberdink said.

"These findings should be considered preliminary," she said. "Patients and physicians must be very careful not to over-interpret them. We don't know why there are more brain hemorrhages in these patients or what the relationship with AMD might be. This does not mean that all patients with late-stage AMD will develop brain hemorrhage."

Beginning in 1990, the Rotterdam Study is a prospective, population-based cohort investigation into factors that determine the occurrence of cardiovascular, neurological, ophthalmological, endocrinological and psychiatric diseases in older people.

The researchers tallied stroke incidence among 6,207 participants 55 years and older. All of the participants were stroke-free at the study's outset. AMD was assessed during scheduled eye examinations, and participants with the condition were divided into five different stages of AMD, and whether their condition was wet AMD or dry AMD. Participants were tracked for an average of 13 years. Of the 726 persons who suffered a stroke in that time, 397 were brain infarctions, 59 were brain hemorrhages and the stroke type was not available for 270.

Late AMD (stage 4) was associated with a 56 percent increased risk of any type of stroke. Late AMD, both the dry and the wet form, was strongly associated with more than six times the risk of brain hemorrhage, but not with brain infarction. Early AMD (stages 1-3) did not increase the risk of any stroke. Associations were adjusted for possible confounders, such as diabetes, blood pressure, anti-hypertensive medications, smoking status, body mass index, alcohol use and C-reactive protein levels.

"We cannot yet say if there is a common causal pathway or mechanism of action yet -- this association needs to be further investigated," Wieberdink said. "But I don't think it is a causal relationship. It seems more likely that late AMD and brain hemorrhage both result from some as yet unknown common mechanism."

If the findings are replicated, it may be possible to develop some stratification of risk among such patients, Wieberdink said.

Co-authors are: Lintje Ho, M.D.; Kamran Ikram, M.D., Ph.D.; Peter Koudstaal, M.D., Ph.D.; Albert Hofman, M.D., Ph.D.; Hans Vingerling, M.D., Ph.D.; and Monique Breteler, M.D., Ph.D. Author disclosers and funding information are on the abstract.

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Ischemic stroke hospitalizations decline in middle-aged, elderly, increases in young

ScienceDaily (Feb. 9, 2011) — The number of acute ischemic stroke hospitalizations among middle-aged and older men and women fell between 1994 and 2007, but sharply increased among those under age 35 -- including teens and children -- according to research presented at the American Stroke Association's International Stroke Conference 2011.

See Also:Health & MedicineStroke PreventionHeart DiseaseElder CareMind & BrainStrokeCaregivingBrain InjuryReferenceMulti-infarct dementiaStrokePeripheral visionCoronary heart disease

Analysts at the U.S. Centers for Disease Control and Prevention (CDC), reviewing hospitalization data by age and gender, identified declining rates of 51 percent in girls 0-4 years and 25 percent in men and 29 percent in women over 45.

However, the number of ischemic stroke hospitalizations increased 51 percent in males between ages 15 and 34 during the period studied. The rate increased 17 percent in females between 15 and 34.

Among children and teens, they found a 31 percent increase in boys between 5 to 14 years and a 36 percent increase among girls 5 to 14 years.

Among the younger middle-aged set, they found a 47 percent increase among men 35-44 and a 36 percent increase among women 35-44.

"I believe this is the first large study to report these findings, stratified by age and gender," said Xin Tong, M.P.H., a health statistician with the CDC's Division for Heart Disease and Stroke Prevention in Atlanta.

"We cannot link anything in particular to the trend in younger patients, but I believe the role of obesity and hypertension will prompt a big discussion. Unfortunately, right now we can't speculate on the causes."

The unit of analysis was hospitalization, so researchers couldn't draw any firm connections or determine what factors are driving the increase in ischemic stroke cases among the young. Ischemic stroke occurs when blood supply to the brain becomes obstructed, usually by a clot or narrowing of the arteries. The risk of long-term brain damage can be reduced significantly if patients receive the clot-busting tissue plasminogen activator (tPA) within three or four and a half hours after stroke onset.

Hospitals and physicians should be aware of the rising risk of stroke in young people, and the necessity to educate them about stroke symptoms, Tong said.

"Acute ischemic stroke is currently considered something that mostly happens to older people, but awareness of rising rates in the young is important or else tPA and other important stroke treatment may be unnecessarily delayed in younger patients," she said.

Tong said her group is pursuing additional investigation on this subject.

Co-authors are: Elena V. Kuklina, M.D., Ph.D.; Cathleen Gillespie, M.S.; and Mary G. George, M.D., M.S.P.H.

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New hybrid drug, derived from common spice, may protect, rebuild brain cells after stroke

ScienceDaily (Feb. 11, 2011) — Whether or not you're fond of Indian, Southeast Asian and Middle Eastern food, stroke researchers at Cedars-Sinai Medical Center think you may become a fan of one of their key spices.

See Also:Health & MedicineStroke PreventionHeart DiseaseMind & BrainBrain InjuryStrokePlants & AnimalsBiologyMiceReferenceMulti-infarct dementiaBrain damageStrokePeripheral vision

The scientists created a new molecule from curcumin, a chemical component of the golden-colored spice turmeric, and found in laboratory experiments that it affects mechanisms that protect and help regenerate brain cells after stroke. Research scientist Paul A. Lapchak, Ph.D., director of Translational Research in the Department of Neurology at Cedars-Sinai Medical Center, is presenting these findings at the American Heart Association International Stroke Conference in Los Angeles.

Only one drug is now approved for ischemic stroke, which occurs when a clot blocks blood flow to the brain. Commonly called a "clot-busting drug," tissue plasminogen activator (tPA) is injected intravenously to dissolve clots and reinstate blood flow. If blood and oxygen are restored in time, consequences of the stroke, such as speech, memory, movement and other impairments, may be reduced.

The new curcumin-hybrid compound -- CNB-001 -- does not attack clots but instead repairs stroke damage at the molecular level that feed and support the all-important brain cells, neurons.

Curcumin has been studied for its potential to treat brain injury and disease, and while the substance itself looks promising, it has several drawbacks, especially as an emergency stroke treatment, which must be quick to be effective: It is not well absorbed in the body, fails to reach its target in high concentrations, becomes depleted quickly, and is blocked from entering the brain by a natural protective mechanism called the blood-brain barrier.

"CNB-001 has many of the same benefits of curcumin but appears to be a better choice of compound for acute stroke because it crosses the blood-brain barrier, is quickly distributed in the brain, and moderates several critical mechanisms involved in neuronal survival," Lapchak says, adding that he and his colleagues expect the new drug to move to human clinical trials soon.

When brain tissue is deprived of blood and oxygen, a cascading series of interrelated events triggers at the molecular level, breaking down the normal electrical and chemical "signaling pathways" responsible for nourishing and supporting neurons. The environment quickly becomes toxic, killing brain cells and destroying their support structures.

Theoretically, interrupting these harmful events and restoring normal pathway function could prevent cell death and the memory and behavioral deficits that result, but it will take a cocktail of drugs or a drug capable of targeting many mechanisms to correct the many pathways damaged by stroke, Lapchak says. CNB-001protects brain cells from damage by repairing four major pathways. One mechanism also plays a major role in the growth and survival of neurons.

The drug reduced stroke-caused "motor deficits" -- problems of muscle and movement control -- in this laboratory study. It was effective when administered up to an hour after stroke, which correlates with about three hours in humans, the same time frame for which tPA is currently approved.

Lapchak and colleagues at the Salk Institute for Biological Studies used the same laboratory rabbit model to mimic human stroke that earlier researchers had employed before the clot-busting drug tPA entered clinical trials. Patrick D. Lyden, M.D., chairman of Cedars-Sinai's Department of Neurology, helped lead a major trial that resulted in the Food and Drug Administration's 1996 approval of tPA, still considered the stroke treatment gold standard.

Those who cook Indian, Thai, Malay and Persian dishes know turmeric well for its zesty flavor, use in curries and for the rich color it imparts to food. Turmeric also has a long history of use in Ayurvedic and Chinese traditional medicine.

Grants from the National Institute of Neurological Disorders and Stroke, part of the National Institutes of Health, supported the CNB-001 study (NS060685 to PAL).

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Sunday, May 29, 2011

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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Gene variant affects stroke prognosis in humans

ScienceDaily (Mar. 1, 2011) — A small difference in DNA sequence predicts the degree of disability after a stroke, according to a paper published online on February 28 in the Journal of Experimental Medicine. Stroke, the consequence of disturbed blood flow to the brain, can impair speech, movement and vision, but it is currently difficult for clinicians to predict the severity of these side effects or the long-term prognosis.

See Also:Health & MedicineStroke PreventionHeart DiseaseElder CareMind & BrainCaregivingBrain InjuryStrokeReferenceBrain damageMulti-infarct dementiaPeripheral visionStroke

Strokes result in the death of brain cells called neurons. Angeles Almeida and co-workers found that variations in a gene known to control cell death -- Tp53 -- influence stroke outcome.

Tp53 comes in two flavors in humans: R and P. The R variant triggers cell death more efficiently. In two distinct groups of stroke patients, those exclusively expressing the R variant suffered more severe disability several months after the stroke. Neurons expressing the R variant were more vulnerable to death caused by oxygen deprivation, a condition that mimics the brain environment during stroke.

Future work is needed to determine if this Tp53 variation can also predict prognosis of patients with other disorders characterized by neuronal death, such as Alzheimer's or Parkinson's disease.

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Wednesday, May 25, 2011

Improved recovery of motor function after stroke

ScienceDaily (Apr. 20, 2011) — After the acute treatment window closes, the only effective treatment for stroke is physical/occupational therapy. Now scientists from Children's Hospital Boston report a two-pronged molecular therapy that leads to significant recovery of skilled motor function in a rat model of stroke. Their findings are reported April 20 in the Journal of Neuroscience.

See Also:Health & MedicineNervous SystemDisabilityStroke PreventionMind & BrainBrain InjuryNeuroscienceCaregivingReferencePhantom limbSensory neuronBrain damagePupillary reflex

By combining two molecular therapies -- each known to promote some recovery on its own -- the researchers achieved more nerve growth and a greater recovery of motor function than with either treatment alone. One therapy, inosine, is a naturally-present molecule that promotes nerve growth; the other is NEP1-40, an agent that counteracts natural inhibitors of nerve growth.

"When you put these two together, you get much stronger growth of new circuits than either one alone, and very striking functional improvements," says senior author Larry Benowitz, PhD, of the Children's Department of Neurosurgery.

Strokes in humans often damage the motor cortex on one side of the brain, interfering with skilled motor functions on the opposite side of the body. Led by Laila Zai, PhD, a postdoctoral fellow in Benowitz's lab and the study's first author, the researchers modeled this scenario by inducing strokes on one side of the rats' brains -- specifically in a part of the motor cortex that controls forelimb movement. They then examined the rats' ability to perform a skilled reaching task -- retrieving food -- with the forelimb on the opposite side.

After 3 to 4 weeks, rats treated with both inosine and NEP1-40 could perform the task -- which required coordinated movements of the paw and digits -- with success rates equivalent to those before the stroke. Benowitz likens the complexity of this task to a person eating with utensils or operating a joystick.

Benowitz has three issued US patents and several US and foreign patent applications pending for the use of inosine to treat stroke, spinal cord injury and traumatic brain injury, and a pending patent application for the inosine/NEP1-40 combined treatment of CNS injury. Earlier studies from his lab, including one published in 2002 and another published last year, demonstrated that inosine encourages nerve fibers to grow from the uninjured side of the brain into regions of the spinal cord that have lost nerve fibers due to stroke. This compensatory rewiring of neural circuits was matched by functional improvements. A separate 2007 study from the University of Cambridge also found that inosine promotes recovery of skilled motor function following traumatic brain injury in rats.

Inosine works by activating a key regulator of nerve growth (an enzyme known as Mst3b). It has a history of safe usage in humans -- it is widely available as a nutritional supplement, and is currently being investigated in clinical trials for the treatment of multiple sclerosis and Parkinson's disease.

NEP1-40 complements inosine's effects by counteracting molecules outside of nerve cells that inhibit nerve growth. Specifically, it blocks signaling through the Nogo receptor, shown by a number of studies to promote the rewiring of neural circuits and to improve functional recovery after stroke.

Benowitz believes circuit rewiring is a promising approach to treating stroke because that is what is thought to underlie the recovery that happens naturally. People with strokes often do regain some function that correlates with shifts in activity to the uninjured parts of the brain. In animal studies, these shifts in brain activity correlate with the growth of new branches from uninjured nerve fibers.

The researchers also found that inosine administered together with environmental enrichment (a model for physical/occupational therapy in humans) led to greater recovery of both nerve growth and motor function. "Physical/occupational therapy should always be part of the strategy," Benowitz says.

The study was funded by the National Institutes of Health, Alseres Pharmaceuticals and the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation (AMRF).

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