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August 19th

Novel Chinese Herbal Medicine Improves Spinal Cord Injury Outcomes in Rats

A new study, published online on June 12, 2013 in Restorative Neurology and Neuroscience, demonstrates that the Chinese herbal medicine Ji-Sui-Kang (JSK), given systemically for three weeks after injury in rats, improved locomotor function, reduced tissue damage, and preserved the structure of neural cells compared to control rats. The report also includes data showing that JSK may first act to reduce inflammation and cell apoptosis and death, and boost local oxygen supply while, later on, it appears to restore function and promote tissue regeneration. Although Chinese herbal medicines have traditionally been used for a variety of ailments, the rationale for their use relies more on anecdotal evidence than the results of modern-day controlled experiments. "A number of anecdotal reports from Chinese medicine practitioners indicate that treatment with a novel herbal formulation, JSK, for periods of one week or three months improved functional recovery," explains co-lead investigator Shucui Jiang, M.D., Ph.D., head of the Hamilton NeuroRestorative Group at McMaster University in Hamilton, Ontario, Canada. "Our present study provides an important and necessary foundation for further studies of JSK." In this study, rats began JSK treatment immediately after undergoing spinal cord injury. Within 7 days, hindlimb locomotor function was significantly better in JSK-treated rats compared to those receiving only saline. JSK-treated rats continued to have better motor function than controls throughout the 21-day test period and treated animals appeared to support their weight better and have more coordinated movements.

June 22nd

Alzheimer's-Disease-Associated Protein Controls Movement in Mice

Researchers in Berlin and Munich, Germany and Oxford, United Kingdom, have revealed that a protein well known for its role in Alzheimer's disease controls spindle development in muscle and leads to impaired movement in mice when the protein is absent or treated with inhibitors. The results, which were published online on June 21, 2013 in an open-access article in The EMBO Journal, suggest that drugs under development to target the beta-secretase-1 protein, which may be potential treatments for Alzheimer's disease, might produce unwanted side effects related to defective movement. Alzheimer's disease is the most common form of dementia found in older adults. The World Health Organization estimates that approximately 18 million people worldwide have Alzheimer's disease. The number of people affected by the disease may increase to 34 million by 2025. Scientists know that the protein beta-secretase-1 or Bace1, a protease enzyme that breaks down proteins into smaller molecules, is involved in Alzheimer's disease. Bace1 cleaves the amyloid precursor protein and generates the damaging Abeta peptides that accumulate as plaques in the brain leading to disease. Now scientists have revealed in more detail how Bace1 works. "Our results show that mice that lack Bace1 proteins or are treated with inhibitors of the enzyme have difficulties in coordination and walking and also show reduced muscle strength," remarked Dr. Carmen Birchmeier, one of the authors of the paper, Professor at the Max-Delbrück-Center for Molecular Medicine in Berlin, Germany, and an EMBO Member. "In addition, we were able to show that the combined activities of Bace1 and another protein, neuregulin-1 or Nrg1, are needed to sustain the muscle spindles in mice and to maintain motor coordination." Muscle spindles are sensory organs that are found throughout the muscles of vertebrates.

May 5th

Genetics of Pulmonary Fibrosis

Researchers from the University of Colorado Denver and colleagues have carried out a genome-wide association study to identify susceptibility loci for fibrotic idiopathic pneumonia. Their results sugget that genes involved in host defense, cell-cell adhesion, and DNA repair contribute to risk for this disease. Specifically, the scientists confirmed association with TERT at 5p15, MUC5B at 11p15, and the 3q26 region near TERC. In addition, they identified seven newly associated loci: FAM13A at 4q22, DSP at 6p24, OBFC1 at 10q24, ATP11A at 13q34,DPP9 at 19p13, and chromosomal regions 7q22 and 15q14-15. The results of this study were published online in Nature Genetics on April 14, 2013. [Nature Genetics abstract]

Why Dense Breasts Predispose to Metastasis in Breast Cancer

Researchers at Washington University School of Medicine in St. Louis have discovered why breast cancer patients with dense breasts are more likely than others to develop aggressive tumors that spread. The finding opens the door to drug treatments that may prevent metastasis. It has long been known that women with denser breasts are at higher risk for breast cancer. This greater density is caused by an excess of a structural protein called collagen. "We have shown how increased collagen in the breasts could increase the chances of breast tumors spreading and becoming more invasive," says Gregory D. Longmore, M.D., professor of medicine. "It doesn't explain why women with dense breasts get cancer in the first place. But once they do, the pathway that we describe is relevant in causing their cancers to be more aggressive and more likely to spread." The results were published online on May 5, 2013 in Nature Cell Biology. Working in mouse models of breast cancer and with breast tumor samples from patients, Dr. Longmore and his colleagues showed that a protein that sits on the surface of tumor cells, called DDR2, binds to collagen and activates a multi-step pathway that encourages tumor cells to spread. "We had no idea DDR2 would do this," says Dr. Longmore, also professor of cell biology and physiology. "The functions of DDR2 are not well understood, and it has not been implicated in cancer -- and certainly not in breast cancer -- until now.” At the opposite end of the chain of events initiated by DDR2 is a protein called SNAIL1, which has long been associated with breast cancer metastasis. Dr. Longmore and his colleagues found that DDR2 is one factor helping to maintain high levels of SNAIL1 inside a tumor cell's nucleus, a necessary state for a tumor cell to spread.

Epileptic Seizures Halted in Mouse Model

University of California San Francisco (UCSF) cell therapy raises hope for severe human forms of epilepsy. UCSF scientists controlled seizures in epileptic mice with a one-time transplantation of medial ganglionic eminence (MGE) cells, which inhibit signaling in overactive nerve circuits, into the hippocampus, a brain region associated with seizures, as well as with learning and memory. Other researchers had previously used different cell types in rodent cell transplantation experiments and failed to stop seizures. Cell therapy has become an active focus of epilepsy research, in part because current medications, even when effective, only control symptoms and not underlying causes of the disease, according to Scott C. Baraban, Ph.D., who holds the William K. Bowes Jr. Endowed Chair in Neuroscience Research at UCSF and led the new study. In many types of epilepsy, he said, current drugs have no therapeutic value at all. "Our results are an encouraging step toward using inhibitory neurons for cell transplantation in adults with severe forms of epilepsy," Dr. Baraban said. "This procedure offers the possibility of controlling seizures and rescuing cognitive deficits in these patients." The findings, which are the first ever to report stopping seizures in mouse models of adult human epilepsy, were published online on May 5, 2013 in Nature Neuroscience. During epileptic seizures, extreme muscle contractions and, often, a loss of consciousness can cause seizure sufferers to lose control, fall, and sometimes be seriously injured. The unseen malfunction behind these effects is the abnormal firing of many excitatory nerve cells in the brain at the same time.

May 4th

New Marker Identified for Sleep Loss

For years, Paul Shaw, Ph .D., a researcher at Washington University School of Medicine in St. Louis, has used what he learns in fruit flies to look for markers of sleep loss in humans. Dr. Shaw reverses the process in a new paper, taking what he finds in humans back to the flies and gaining new insight into humans as a result: identification of a human gene that is more active after sleep deprivation. “I’m calling the approach cross-translational research,” says Dr. Shaw, associate professor of neurobiology. “Normally we go from model to human, but there’s no reason why we can’t take our studies from human to model and back again.” Dr. Shaw and his colleagues plan to use the information they are gaining to create a panel of tests for sleep loss. The tests may one day help assess a person’s risk of falling asleep at the wheel of a car or in other dangerous contexts. PLOS ONE published the results online on April 24, 2013. Scientists have known for years that sleep disorders and disruption raise blood serum levels of interleukin 6, an inflammatory immune compound. Dr. Shaw showed that this change is also detectable in saliva samples from sleep-deprived rats and humans. Based on this link, Shaw tested the activity of other immune proteins in humans to see if any changed after sleep loss. The scientists took saliva samples from research participants after they had a normal night’s sleep and after they stayed awake for 30 hours. They found two immune genes whose activity levels rose during sleep deprivation. “Normally we would do additional human experiments to verify these links,” Dr. Shaw says.