Newsline — Wednesday, July 16, 2014 13:00
Social Behavior Tied to Activity in Specific Brain Circuit
Study: Brain Bleed Outcomes No Worse With Dabigatran
Wednesday, July 16, 2014 9:00
A retrospective study out of the University of Minnesota, recently reported online in Stroke and discussed in a MedPageToday article, showed that the prognosis from intracranial bleeding did not appear to be poorer among patients with atrial fibrillation who are taking dabigatran (Pradaxa) instead of warfarin. The findings were consistent with a prior analysis of the RE-LY trial. Although dabigatran and the other novel oral anticoagulants have been shown to reduce the rate of intracranial hemorrhage relative to warfarin in clinical trials, there are lingering concerns that patients who have an intracranial bleed might do worse with one of the newer agents because of the lack of reversal agents. To read the full article, click here.
Potential Alzheimer’s Drug Prevents Abnormal Blood Clots in the Brain
Tuesday, July 15, 2014 15:26
New experiments at Rockefeller University have identified a compound that might halt the progression of Alzheimer’s disease by interfering with the role amyloid-β plays in the formation of blood clots. By targeting the protein’s ability to bind to a clotting agent in blood, the researchers’ work offers a promising new strategy, according to the study published in Nature Reviews Drug Discovery. This latest study builds on previous work in lab showing amyloid-β can interact with fibrinogen to form difficult-to-break-down clots that alter blood flow, cause inflammation and choke neurons. “Our experiments in test tubes and in mouse models of Alzheimer’s showed the compound, known as RU-505, helped restore normal clotting and cerebral blood flow. But the big pay-off came with behavioral tests in which the Alzheimer’s mice treated with RU-505 exhibited better memories than their untreated counterparts,” said Sidney Strickland. “These results suggest we have found a new strategy with which to treat Alzheimer’s disease.” To learn more about the study, click here.
Blocking Key Enzyme Minimizes Stroke Injury
Monday, July 14, 2014 17:29
A drug that blocks the action of the enzyme Cdk5 could substantially reduce brain damage if administered shortly after a stroke, UT Southwestern Medical Center research suggests. The findings, recently reported in the Journal of Neuroscience, determined in rodent models that aberrant Cdk5 activity causes nerve cell death during stroke. More importantly, development of a Cdk5 inhibitor as an acute neuroprotective therapy has the potential to reduce stroke injury. In this study, researchers administered a Cdk5 inhibitor directly into dissected brain slices after adult rodents suffered a stroke, in addition to measuring the post-stroke effects in Cdk5 knockout mice. “If you inhibit Cdk5, then the vast majority of brain tissue stays alive without oxygen for up to one hour,” said Dr. James Bibb, senior author of the study. “This result tells us that Cdk5 is a central player in nerve cell death.” To learn more about the study, click here.
3-D Computer Model for Deep Brain Stimulation to Treat Dystonia
Friday, July 11, 2014 9:00
Although deep brain stimulation (DBS) can be an effective therapy for dystonia, the treatment isn’t always effective, or benefits may not be immediate. Precise placement of DBS electrodes is one of several factors that can affect results, but few studies have attempted to identify where electrode placement is most effective. Researchers have now created 3-D, computerized models that map the brain region involved in dystonia. In this retrospective study, investigators examined a database of 94 patients with the most common genetic form of dystonia, DYT1, who had been treated with DBS for at least a year. They selected 21 patients who had good responses to treatment, compiled their demographic and treatment information, and used magnetic resonance imaging scans to create 3-D anatomical models with a fine grid to show exact location of relevant brain structures. The investigators then simulated the placement of electrodes as they were positioned in the patients’ brains and input the actual stimulation parameters into a computer program, which calculated detailed information specific to each patient and each electrode. “We found that…
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Study: TBI in Veterans May Increase Risk of Dementia
Thursday, July 10, 2014 13:29
Older veterans who have experienced a traumatic brain injury (TBI) are 60 percent more likely to later develop dementia than veterans without TBI, according to a study recently published online in Neurology. The study also found that veterans with a history of TBI developed dementia about two years earlier than those without TBI who had developed dementia. The study involved 188,784 veterans with an average age of 68 at the start of the study. All were free of dementia at the start of the study and had at least one visit to a Veterans Affairs health-care facility at the start of the study and again an average of seven years later. A total of 1,229 of the veterans had a TBI diagnosis. During the follow-up period, 16 percent of veterans with TBI developed dementia. After adjusting for other factors that could affect the risk of dementia, researchers determined that veterans with TBI were 60 percent more likely to develop dementia than those without TBI. The researchers also found that the risk of dementia was higher…
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Cocoa Extract May Counter Specific Mechanisms of Alzheimer’s
Wednesday, July 9, 2014 13:00
A specific preparation of cocoa-extract called Lavado may reduce damage to nerve pathways seen in Alzheimer’s disease patients’ brains long before they develop symptoms, according to a study conducted at the Icahn School of Medicine at Mount Sinai. Specifically, the study results, recently published in the Journal of Alzheimer’s Disease, using mice genetically engineered to mimic Alzheimer’s disease, suggest that Lavado cocoa extract prevents the protein β-amyloid- (Aβ) from gradually forming sticky clumps in the brain. The theory is that Aβ oligomers physically interfere with synaptic structures and disrupt mechanisms that maintain memory circuits’ fitness. In addition, Aβ triggers immune inflammatory responses. Lavado cocoa is primarily composed of polyphenols. Evidence in the current study is the first to suggest that adequate quantities of specific cocoa polyphenols in the diet over time may prevent the glomming together of Aβ into oligomers that damage the brain. The research team tested the effects of extracts from Dutched, natural and Lavado cocoa, which contain different levels of polyphenols. Each cocoa type was evaluated for its ability to reduce the…
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Fatal Cellular Malfunction Identified in Huntington’s Disease
Wednesday, July 9, 2014 9:00
Researchers believe they have learned how mutations in the gene that causes Huntington’s disease kill brain cells. A study, reported online in Nature Neuroscience, found in mice and in mouse brain cell cultures that the disease impairs the transfer of proteins to mitochondria, causing brain cell death. Huntington’s disease is caused by a defect in the huntingtin gene, which makes the huntingtin protein. Scientists have known for some time that the mutated form of the huntingtin protein impairs mitochondria and that this disruption kills brain cells. But they have had difficulty understanding specifically how the gene harms the mitochondria. In this new study, researchers found that the mutated huntingtin protein binds to TIM23, a protein complex that normally helps transfer essential proteins and other supplies to the mitochondria, but the mutated huntingtin protein impairs that process — a problem that seems to be specific to brain cells early in the disease. To learn more about the study, click here.
Early Life Stress Can Leave Lasting Impacts on the Brain
Tuesday, July 8, 2014 13:00
A team of University of Wisconsin-Madison researchers recently showed that toxic stressors, such as poverty, neglect and physical abuse, experienced in early life, might be changing the parts of developing children’s brains responsible for learning, memory and the processing of stress and emotion. For the study, published in Biological Psychiatry, the team recruited 128 children around age 12 who had experienced either physical abuse, neglect early in life or came from low socioeconomic status households. Researchers conducted extensive interviews with the children and their caregivers, and also took images of the children’s brains, focusing on the hippocampus and amygdala. The images then were compared to similar children from middle-class households who had not been maltreated. Indeed, their hand measurements found that children who experienced any of the three types of early life stress had smaller amygdalas than children who had not. Children from low socioeconomic status households and children who had been physically abused also had smaller hippocampal volumes. To learn more about this study, click here.
How Aging Can Intensify Damage of Spinal Cord Injury
Monday, July 7, 2014 13:17
Researchers from The Ohio State University have found that in spinal cord injury, immune cells in the central nervous system of elderly mice fail to activate an important signaling pathway, dramatically lowering chances for repair after injury. These animal studies, published in the Journal of Neuroscience, show that spinal cord injuries are more severe in elderly mice than in young adults. A key messenger in that pathway is a receptor on the surface of microglia. In young adult mice, this receptor is activated by microglia to recognize and make use of an inflammation-related signaling chemical that is found in the central nervous system after a spinal cord injury. The microglia in the elderly mice, however, do not activate the receptor at all. The study showed that the difference in receptor activation has consequences later in the recovery process. The lesions on the injured spinal cord were 38 percent longer, on average, in elderly mice than in young adult mice. In addition, the older mice were unable to gain movement of their hind limbs by the…
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