Posts tagged science
Articles and news from the latest research reports.
Cigarette smoking increases the risk of subarachnoid hemorrhage (SAH) in a dose-responsive manner, and cessation correlates with a reduction in SAH risk, according to a study published online Aug. 30 in the Journal of Neurology, Neurosurgery & Psychiatry.
To examine the risk of SAH in relation to smoking cessation, Chi Kyung Kim, M.D., from Seoul National University Hospital in Korea, and colleagues performed a nationwide multicenter case control study involving 426 SAH patients and 426 matched controls. Structured questionnaires were used to assess lifestyle, medical history, and smoking habits.
The researchers found that 37.4 percent of SAH patients and 24.2 percent of controls were current smokers (adjusted odds ratio, 2.84), after adjusting for potential confounders. The risk of SAH was found to increase in a dose-responsive fashion with cumulative dose of smoking (pack years). There was a significant reduction in SAH to 59 percent with smoking cessation (at least five years). A history of heavy smoking (at least 20 cigarettes per day) correlated with a 2.3-fold increased risk of SAH, compared with participants who had never smoked (P < 0.05).
"We have demonstrated that cigarette smoking increases the risk of SAH, but smoking cessation decreases the risk in a time-dependent manner, although this beneficial effect may be diminished in previous heavy smokers," the authors write. "To forestall tragic SAH events, our results call for more global and vigorous efforts for people to stop smoking."
Results of a study led by researchers at Boston University School of Medicine (BUSM) and the Veterans Affairs (VA) Boston Healthcare System indicate that the proposed changes to the diagnosis of post-traumatic stress disorder (PTSD) will not substantially affect the number of people who meet criteria for the disorder.
The Diagnostic and Statistical Manual of Mental Disorders (DSM), the handbook that defines psychiatric disorders, has been undergoing revisions for the past decade in advance of the publication of its fifth edition (DSM-5). Included in the proposed revisions are the first major changes to the PTSD diagnosis since its initial appearance in DSM-III back in 1980. These include the addition of new symptoms, revision of existing ones and a new set of diagnostic criteria.
According to DSM-IV, the criteria for a diagnosis of PTSD include exposure to a traumatic event, persistent re-experiencing of the traumatic event, avoidance and emotional numbing, and persistent hyperarousal and hypervigilance. The proposed revisions for DSM-5 involve clarification regarding what constitutes a traumatic event, the addition symptoms such as self-destructive behavior and distorted blaming of oneself or others for the traumatic event and a reorganization of the diagnostic decision rules for establishing a diagnosis of PTSD.
New algorithm can analyze information from medical images to identify diseased areas of the brain and connections with other regions.
Disorders such as schizophrenia can originate in certain regions of the brain and then spread out to affect connected areas. Identifying these regions of the brain, and how they affect the other areas they communicate with, would allow drug companies to develop better treatments and could ultimately help doctors make a diagnosis. But interpreting the vast amounts of data produced by brain scans to identify these connecting regions has so far proved impossible.
Now, researchers in the Computer Science and Artificial Intelligence Laboratory at MIT have developed an algorithm that can analyze information from medical images to identify diseased areas of the brain and their connections with other regions.
The MIT researchers will present the work next month at the International Conference on Medical Image Computing and Computer Assisted Intervention in Nice, France.
Having access to a personal computer lowers or decreases the risk of cognitive decline and dementia in older men by up to 40 per cent, according to researchers at The University of Western Australia.
Winthrop Professor Osvaldo Almeida and his colleagues undertook an eight-year study of more than 5000 Perth men aged from 65 to 85. The results are published in the journal PLoSOne.
Study in mice suggests sleep problems may be early sign of Alzheimer’s
September 5, 2012 by Michael C. Purdy
Sleep disruptions may be among the earliest indicators of Alzheimer’s disease, scientists at Washington University School of Medicine in St. Louis report Sept. 5 in Science Translational Medicine.
Working in a mouse model, the researchers found that when the first signs of Alzheimer’s plaques appear in the brain, the normal sleep-wake cycle is significantly disrupted.
“If sleep abnormalities begin this early in the course of human Alzheimer’s disease, those changes could provide us with an easily detectable sign of pathology,” says senior author David M. Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of Washington University’s Department of Neurology. “As we start to treat Alzheimer’s patients before the onset of dementia, the presence or absence of sleep problems may be a rapid indicator of whether the new treatments are succeeding.”
Holtzman’s laboratory was among the first to link sleep problems and Alzheimer’s through studies of sleep in mice genetically altered to develop Alzheimer’s plaques as they age. In a study published in 2009, he showed that brain levels of a primary ingredient of the plaques naturally rise when healthy young mice are awake and drop after they go to sleep. Depriving the mice of sleep disrupted this cycle and accelerated the development of brain plaques.
A similar rising and falling of the plaque component, a protein called amyloid beta, was later detected in the cerebrospinal fluid of healthy humans studied by co-author Randall Bateman, MD, the Charles F. and Joanne Knight Distinguished Professor of Neurology at Washington University.
The new research, led by Jee Hoon Roh, MD, PhD, a neurologist and postdoctoral fellow in Holtzman’s laboratory, shows that when the first indicators of brain plaques appear, the natural fluctuations in amyloid beta levels stop in both mice and humans.
“We suspect that the plaques are pulling in amyloid beta, removing it from the processes that would normally clear it from the brain,” Holtzman says.
Mice are nocturnal animals and normally sleep for 40 minutes during every hour of daylight, but when Alzheimer’s plaques began forming in their brains, their average sleep times dropped to 30 minutes per hour.
To confirm that amyloid beta was directly linked to the changes in sleep, researchers gave a vaccine against amyloid beta to a new group of mice with the same genetic modifications. As these mice grew older, they did not develop brain plaques. Their sleeping patterns remained normal and amyloid beta levels in the brain continued to rise and fall regularly.
Scientists now are evaluating whether sleep problems occur in patients who have markers of Alzheimer’s disease, such as plaques in the brain, but have not yet developed memory or other cognitive problems.
“If these sleep problems exist, we don’t yet know exactly what form they take—reduced sleep overall or trouble staying asleep or something else entirely,” Holtzman says. “But we’re working to find out.”
(Source: news.wustl.edu)
Scientists have found that eliminating an enzyme from mice with symptoms of Alzheimer’s disease leads to a 90 percent reduction in the compounds responsible for formation of the plaques linked to this form of dementia — the most dramatic reduction in this compound reported to date in published research.
After a summer marred by disappointing clinical-trial results in patients with Alzheimer’s disease, drug developers are regrouping to plot a fresh course in the battle against the devastating disorder.
The bad news began in July and August, when Johnson & Johnson and Pfizer learned that their biological drug bapineuzumab had failed to show any benefit in two large trials. Then, on 24 August, Eli Lilly said that its drug solanezumab had not hit its goal of significantly slowing the memory decline and dementia that characterize Alzheimer’s disease.
Both of the failed drugs targeted amyloid-β, a protein that forms plaques in the brains of patients with the disease and that has long been the prime suspect for causing it. But rather than abandoning the amyloid hypothesis, scientists are pinning their hopes on innovative clinical-trial designs and new diagnostics that would allow them to test compounds earlier in the disease and gauge their efficacy more quickly.
Can simply describing your feelings at stressful times make you less afraid and less anxious? A new UCLA psychology study suggests that labeling your emotions at the precise moment you are confronting what you fear can indeed have that effect.
Scientists on the Florida campus of The Scripps Research Institute have designed a compound that shows promise as a potential therapy for one of the diseases closely linked to fragile X syndrome, a genetic condition that causes mental retardation, infertility, and memory impairment, and is the only known single-gene cause of autism.
The study, published online ahead of print in the journal ACS Chemical Biology September 4, 2012, focuses on tremor ataxia syndrome, which usually affects men over the age of 50 and results in Parkinson’s like-symptoms—trembling, balance problems, muscle rigidity, as well as some neurological difficulties, including short-term memory loss and severe mood swings.
New research finds that the way that the visual centers of men and women’s brains works is different. Men have greater sensitivity to fine detail and rapidly moving stimuli, but women are better at discriminating between colors.