Posts tagged neuroscience
Articles and news from the latest research reports.
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.
A Blueprint for ‘Affective’ Aggression
A North Carolina State University researcher has created a roadmap to areas of the brain associated with affective aggression in mice. This roadmap may be the first step toward finding therapies for humans suffering from affective aggression disorders that lead to impulsive violent acts.
Affective aggression differs from defensive aggression or premeditated aggression used by predators, in that the role of affective aggression isn’t clear and could be considered maladaptive. NC State neurobiologist Dr. Troy Ghashghaei was interested in finding the areas of the brain engaged with this type of aggressive behavior. Using mice that had been specially bred for affective aggression by his research associate Dr. Derrick L Nehrenberg, Ghashghaei and former undergraduate student Atif Sheikh were able to locate the regions in the mouse brain that switched on and those that were off when the mice displayed affective aggression.
“The brain works by using clusters of neurons that cross communicate at extremely rapid rates, much like a computer,” Ghashghaei explains. “One region will process a stimulus, and then that region sends messages to other clusters within the brain, like circuits within a computer. We looked at how the switches flipped in the brains of aggressive mice, and compared that with the brains of completely nonaggressive mice in the same setting, to see how the two processed the situation differently.”
They found that affectively aggressive mice demonstrated a large difference in the way their “executive centers” operated when the mice encountered another mouse. “Sensory inputs come in and are sent to the executive center, the part of the brain that decides how to respond to the input,” Ghashghaei says. “In the meantime, the information about the response you made gets processed back with either a pleasant or unpleasant association.”
According to Ghashghaei, the affectively aggressive mice could react violently because their brains are hardwiredto respond to certain situations aggressively without assessing whether their response to the situation is appropriate or without regard to the behavior’s consequences. In addition, affectively aggressive mice may be forming pleasant associations with their violent displays, which would reinforce their aggressive tendencies.
“We cannot say which of the two possibilities underlie the persistent aggressive displays by our mice,” Ghashghaei says, “but we can see that the patterns of neuronal activity are very different in the executive centers of these mice. Additionally, there are differences in the neuronal clusters involved with creating pleasant or unpleasant associations to the stimulus or their response. That gives us a few starting spots to begin identifying the mechanisms that underlie these profound behavioral differences.”
The regions of the brain that were involved in affective aggression in the mice are similar across all mammalian species. Ghashghaei hopes that his findings in mice will be useful to researchers studying violent behavior in humans, as well as aggression in other animals.
“With the brain, just knowing where to start looking is huge,” Ghashghaei says. “Once you have a few targets, you can tease out the possibilities and get to the heart of the problem. We are confident that manipulation of some of the identified targets in our study will disrupt displays of affective aggression in our mouse model.”
(Source: news.ncsu.edu)
A*STAR scientists have identified a biomarker of the most lethal form of brain tumours in adults − glioblastoma multiforme. The scientists found that by targeting this biomarker and depleting it with a potential drug, they were able to prevent the progression and relapse of the brain tumour.
Researchers have discovered two gene variants that raise the risk of the pediatric cancer neuroblastoma. Using automated technology to perform genome-wide association studies on DNA from thousands of subjects, the study broadens understanding of how gene changes may make a child susceptible to this early childhood cancer, as well as causing a tumor to progress.
“We discovered common variants in the HACE1 and LIN28B genes that increase the risk of developing neuroblastoma. For LIN28B, these variants also appear to contribute to the tumor’s progression once it forms,” said first author Sharon J. Diskin, PhD, a pediatric cancer researcher at The Children’s Hospital of Philadelphia. “HACE1 and LIN28B are both known cancer-related genes, but this is the first study to link them to neuroblastoma.”
Diskin and colleagues, including senior author John M. Maris, MD, director of the Center for Childhood Cancer Research at Children’s Hospital, published the study online Sept. 2 in Nature Genetics.