Posts tagged neuroscience

Posts tagged neuroscience

Fruit Flies On Methamphetamine Die Largely as a Result of Anorexia
The abuse of methamphetamine can have significant harmful side effects in humans. It burdens the body with toxic metabolic byproducts and weakens the heart, muscles and bones. It alters energy metabolism in the brain and kills brain cells.
Previous studies have shown that the fruit fly Drosophila melanogaster is a good model organism for studying the effects of methamphetamine on the body and brain. Researchers have found that meth exposure has similar toxicological effects in fruit flies and in humans and other mammals.

Coffee May Help Some Parkinson’s Disease Movement Symptoms, Research Suggests
"Studies have shown that people who use caffeine are less likely to develop Parkinson’s disease, but this is one of the first studies in humans to show that caffeine can help with movement symptoms for people who already have the disease," said study author Ronald Postuma, MD, MSc, with McGill University in Montreal and the Research Institute of the McGill University Health Center. Postuma is also a member of the American Academy of Neurology.
August 1, 2012
(Medical Xpress) — In work that may revolutionise rehabilitation for stroke patients, researchers from The University of Auckland and the Auckland District Health Board have shown it is possible to predict an individual’s potential for recovery of hand and arm function after a stroke.
The new approach can be used to personalise rehabilitation so that patients and therapists set realistic goals for recovery. It may also improve outcomes of trials that evaluate new therapies, by identifying patients who are most likely to respond to specific treatments.
“One in six people worldwide will have a stroke in their lifetime,” says principal investigator Professor Winston Byblow. “After stroke, impairment of the arm and hand is very common and has a major impact on independence and quality of life.
“Until now it has only been possible to group patients together according to their broad similarity to others who have already gone through upper limb rehabilitation, but this information cannot inform an individual patient’s rehabilitation plan. We have developed the first clinical algorithm to actually predict the individual patient’s potential for recovery based on information gathered before rehabilitation begins.”
The lead author of the study, Dr Cathy Stinear explains: “The algorithm begins with a bedside test within three days of stroke. The test takes only a few minutes and requires no special equipment. This is sufficient to provide a prediction for many patients, but for others an additional test is required to measure the integrity of neural pathways from the brain to the arm. If this test gives no definitive result, an MRI assessment can be performed to better determine whether the pathways in the stroke-damaged side of the brain remain viable.”
The research team have trialled the process in patients and followed their recovery. “When the tests are combined in our stepwise algorithm they accurately predict each patient’s recovery at 12 weeks, which is around the time that therapy normally ends,” says Dr Stinear.
Neurologist Professor Alan Barber, a member of the research team and Head of the Auckland Hospital Stroke Service, says that the findings are very significant. “This is the first study to predict an individual’s potential for motor recovery using measures obtained from that patient in the initial days after stroke. This information can be used to tailor rehabilitation before it begins.”
The team is now involved in a three-year trial of the algorithm within the hospital. The results will show whether the algorithm leads to improved outcomes for patients and increases the efficiency of rehabilitation services.
Provided by University of Auckland
Source: medicalxpress.com
Artificial Butter Flavoring Ingredient Linked to Key Alzheimer’s Disease Process
A new study raises concern about chronic exposure of workers in industry to a food flavoring ingredient used to produce the distinctive buttery flavor and aroma of microwave popcorn, margarines, snack foods, candy, baked goods, pet foods and other products. It found evidence that the ingredient, diacetyl (DA), intensifies the damaging effects of an abnormal brain protein linked to Alzheimer’s disease. The study appears in ACS’ journal Chemical Research in Toxicology.

Alzheimer’s villain cures multiple sclerosis in mice
A notorious biochemical villain has just revealed its heroic side. Beta-amyloid, a misfolded protein fragment blamed for killing brain cells in Alzheimer’s disease, has reversed the symptoms of mice suffering from the rodent equivalent of multiple sclerosis (MS).
MS occurs when the immune system mistakenly attacks the fatty myelin sheaths around nerve fibres that serve as electrical insulation. Without this insulation, nervous impulses falter, leading to physical and cognitive problems. Myelin increases the speed at which electrical impulses travel around the body.
As it is destroyed, nerve communication falters, leading to physical and cognitive problems. Lawrence Steinman of Stanford University in California had expected amyloid-beta to exacerbate this damage, given that it is toxic to neurons and builds up where myelin sheaths are being destroyed.
How the Brain and Nerve Cells Change During Alzheimer’s Disease
One of the hallmarks of Alzheimer’s disease is the accumulation of amyloid plaques between nerve cells (neurons) in the brain. Beta amyloid is a fragment of a protein snipped from another protein called amyloid precursor protein (APP). In a healthy brain, these protein fragments would break down and be eliminated. In Alzheimer’s disease, the fragments accumulate to form hard, insoluble plaques.
Neurofibrillary tangles are insoluble twisted fibers found inside the brain’s nerve cells. They primarily consist of a protein called tau, which forms part of a structure called a microtubule. The microtubule helps transport nutrients and other important substances from one part of the nerve cell to another. Axons are long threadlike extensions that conduct nerve impulses away from the nerve cell; dendrites are short branched threadlike extensions that conduct nerve impulses towards the nerve cell body. In Alzheimer’s disease the tau protein is abnormal and the microtubule structures collapse.
As Alzheimer’s disease spreads through the cerebral cortex (the outer layer of the brain), judgment worsens, emotional outbursts may occur and language is impaired. Memory worsens and may become almost non-existent. On average, those with Alzheimer’s live for 8 to 10 years after diagnosis, but this terminal disease can last for as long as 20 years.

The Aging Brain Is More Malleable Than Previously Believed
There is growing evidence that, beyond what was previously believed, the adult human brain is remarkably malleable and capable of new feats — even in the last decades of life.
In fact, new experiences can trigger major physical changes in the brain within just a few days, and certain conditions can accelerate this physical, chemical and functional remodeling of the brain.
"We used to think that the brain was completely formed by development and its basic structure didn’t change much in adults, but as research went on we discovered that wasn’t true, at least in the cerebral cortex," explains Randy Bruno, a member of the Kavli Institute for Brain Science at Columbia University. "We now know that an underlying portion of the brain called the thalamus, which feeds the cortex information from our senses, is also remarkably plastic."
Researchers map the expression patterns of 1,000 genes in the human brain.
The paper
H. Zeng et al., “Large-scale cellular-resolution gene profiling in human neocortex reveals species-specific molecular signatures,” Cell, 149:48-96, 2012.
The finding
Whole-genome sequencing has given researchers a good sense of which genes are shared between, for example, humans and mice. But little is known about how the expression patterns of these genes differ. Hongkui Zeng of the Allen Institute for Brain Science in Seattle, Washington, and colleagues took slices of human brains collected from postmortem biopsies and tested the expression of 1,000 key neuronal genes. They found that about 21 percent of the gene-expression profiles differed between the two species.
The sliver
Researchers took thin slices from regions of the brain involved in processing visual and sensory information and scanned them for the in situ expression of 1,000 genes that act as markers of cell type or are involved in disease, evolution, or cortical function. They compared gene expression of three areas of the cortex across 46 donors with corresponding mouse-brain slices, which had been analyzed previously at the Allen Institute.
The difference
The differences between humans and mice “often manifested in a cell type-specific way,” said Zeng, or involved in between-cell communications. “The disease genes are all very well conserved,” which bodes well for researchers using mice as models of disease, she says.
The impact
“The mouse model is used extensively in neuroscience research, and it’s assumed to be a surrogate for the human,” says Daniel Geschwind, a neurogeneticist at the University of California, Los Angeles. Knowing the specific differences “gives you a sense that many things are conserved, but also provides some guidance as to the ones that aren’t.”
Sick from Stress? Blame Your Mom… And Epigenetics
If you’re sick from stress, a new research report appearing in the August 2012 issue of The FASEB Journal suggests that what your mother ate — or didn’t eat — may be part of the cause. The report shows that choline intake that is higher than what is generally recommended during pregnancy may improve how a child responds to stress. These improvements are the result of epigenetic changes that ultimately lead to lower cortisol levels. Epigenetic changes affect how a gene functions, even if the gene itself is not changed. Lowering cortisol is important as high levels of cortisol are linked to a wide range of problems ranging from mental health to metabolic and cardiovascular disorders.
ScienceDaily (July 31, 2012) — Research just published by scientists at Cold Spring Harbor Laboratory (CSHL) links gene mutations found in some patients with Meier-Gorlin syndrome (MGS) with specific cellular dysfunctions that are thought to give rise to a particularly extreme version of dwarfism, small brain size, and other manifestations of abnormal growth which generally characterize that rare condition.
Although only 53 cases of Meier-Gorlin syndrome have been reported in the medical literature since the first patient was described in 1959, it is a malady whose mechanisms are bringing to light new functions for some of the cellular processes common to all life. Pathology related to MGS is traced in the new research to one of these, the fundamental process called mitosis in which cells replicate their genetic material and prepare to divide into two identical “daughter” cells.
CSHL President and Professor Bruce Stillman, Ph.D., a cancer biologist who has made seminal discoveries over three decades that have helped reveal the exquisite choreography of how chromosomes are duplicated in cells, led the new research, which suggests how, during mitosis, mutant versions of a protein called Orc1 contribute in two distinct ways to severe MGS pathology. The research is published online ahead of print in Genes & Development.