Posts tagged brain

ScienceDaily (June 11, 2012) — Non-medical prescription drug use by college students is a growing trend on most campuses, according to the U.S. Department of Education’s Higher Education Center for Alcohol, Drug Abuse and Violence Prevention. Due to this trend, Western Illinois University Department of Health Sciences Assistant Professor Amanda Divin and her colleague, Keith Zullig, an associate professor in the West Virginia University School of Public Health, recently conducted and published a study that explores non-medical prescription drug use and depressive symptoms in college students.

Divin and Zullig utilized data from the fall 2008 American College Health Association National College Health Assessment (ACHA-NCHA), a national research survey that addresses seven areas of health and behavior of college students, one of which is alcohol, tobacco and other drug use. The sample used for the study (from the ACHA-NCHA data) contained 26,600 randomly selected college students from 40 campuses in the U.S. The student respondents were asked about their non-medical prescription drug use (including painkillers, stimulants, sedatives and antidepressants) and mental health symptoms within the last year.

According to Divin’s and Zullig’s results, approximately 13 percent of the college-student respondents reported non-medical prescription drug use, with those who reported feeling hopeless, sad, depressed or considered suicide being significantly more likely to report non-medical use of any prescription drug. The results also showed this relationship was more pronounced for females who reported painkiller use. The study — which is titled, “The association between non-medical prescription drug use, depressive symptoms, and suicidality among college students” — will appear in the August 2012 issue of Addictive Behaviors: An International Journal.

"Because prescription drugs are tested by the U.S. Food and Drug Administration and prescribed by a doctor, most people perceive them as ‘safe’ and don’t see the harm in sharing with friends or family if they have a few extra pills left over," Divin explained. "Unfortunately, all drugs potentially have dangerous side effects. As our study demonstrates, use of prescription drugs — particularly painkillers like Vicodin and Oxycontin — is related to depressive symptoms and suicidal thoughts and behaviors in college students. This is why use of such drugs need to be monitored by a doctor and why mental health outreach on college campuses is particularly important."

Divin and Zullig believe the results suggest that students are self-medicating their psychological distress with prescription medications.

"Considering how common prescription sharing is on college campuses and the prevalence of mental health issues during the college years, more investigation in this area is definitely warranted," Divin added. "Our study is just one of the many first steps in exploring the relationship between non-medical prescription drug use and mental health."

Source: Science Daily

ScienceDaily (June 11, 2012) — Sportsmen and women have been known to dope with the blood hormone Epo to enhance their performance. Researchers from the University of Zurich have now discovered, through animal testing, that Epo has a performance-enhancing effect in the brain shortly after an injection by improving oxygen transport in blood. As Epo also increases motivation, it could be useful in treating depression, experts say.

The well-known blood hormone Epo is not only used for medicinal purposes; some athletes misuse it for doping. It boosts the number of red blood cells, thereby increasing the transport of oxygen to the muscles. This leads to improvements in performance, which can especially give endurance athletes such as cyclists or marathon runners the edge.

Epo has immediate impact on exercise performance

In a recently published study, Max Gassmann, a veterinary physiologist from the University of Zurich, proved that Epo also drastically increases motivation in the brain as soon as it has been injected, without the number of red blood cells increasing.

Gassmann’s team tested exercise performance of differently treated mice, studying genetically modified mice that produce human Epo solely in the brain and mice that the researchers had injected with Epo and the hormone reached the brain thus by blood. Both mouse groups exhibited an increased performance on the treadmill compared to the untreated control animals. “We assume that Epo in the brain triggers a motivation boost to increase physical performance,” explains Professor Gassmann. He and his team are now testing the performance-enhancing effect of Epo on volunteers.

Epo probably has an impact on people’s moods, too. It might thus be used in patients who suffer from depression. The latest experiments conducted by a German-Danish research group reveal that Epo can also alleviate the condition of patients suffering from schizophrenia by improving their mental performance.

Source: Science Daily

June 11, 2012

The younger a woman is when she goes through the menopause, the greater may be her risk of having a brain (cerebral) aneurysm, suggests research published online first in the Journal of NeuroInterventional Surgery.

A cerebral aneurysm refers to an abnormal bulging of one of the arteries in the brain, which is often only discovered when it ruptures, causing a potentially fatal and/or disabling bleed.

Women are more prone to cerebral aneurysms than men. And fluctuations in the female hormone oestrogen have been implicated in the development of aneurysms, the incidence of which, along with cardiovascular disease, rises sharply after menopause.

The authors base their findings on 76 postmenopausal women who had had a cerebral aneurysm, which, in most cases had not ruptured, and who were subsequently quizzed about their medical and reproductive histories.

Conditions, such as high blood pressure, diabetes, high cholesterol and an underactive thyroid gland (hypothyroidism) can all boost the risk of a stroke, while the number of pregnancies and the age at which periods start and stop determine lifetime exposure to oestrogen.

This information was then compared with that taken from more than 4,500 women participants of the 2002 National Institute of Child Health and Human Development Contraceptive and Reproductive Experiences Study, and matched for age and educational attainment.

The average age at which women in both groups had started the menopause was similar, and analysis of the results showed that later menopause and use of hormone replacement therapy (HRT) protected against the risk of a cerebral aneurysm, lessening the risk by 21% and 77%, respectively.

Premature menopause - before the age of 40 - had occurred in one in four (26%) of the women who had had an aneurysm compared with around one in five (19%) of those in the comparison group.

And each successive four year increase in the age at which a woman went through the menopause lessened the likelihood of a cerebral aneurysm by around 21%.

Smoking did not seem to be linked to an increase in risk, while alcohol consumption was of borderline significance.

The outcomes for ruptured cerebral aneurysms are poor, with around one in two people who have one likely to die. One in 10 people die before they reach hospital and of those who survive, one in five is severely disabled, say the authors, so finding a potential marker may help to detect the condition earlier.

"Loss of oestrogen earlier in a woman’s life may contribute to the [development] of cerebral aneurysm," conclude the authors, adding that HRT may protect against this. And they suggest: "These data may identify a risk factor for [the development of this condition] and also a potential target for future therapies."

Provided by British Medical Journal

Source: medicalxpress.com

June 11, 2012

The American Academy of Neurology has issued an updated guideline outlining the best treatments for infantile spasms, a rare type of seizure that can occur in infants and young children. The guideline, which was co-developed with the Child Neurology Society, is published in the June 12, 2012, print issue of Neurology, the medical journal of the American Academy of Neurology.

Infantile spasms is a rare disorder that usually begins in infants aged four to six months. The spasms are a type of seizure that mainly consists of a sudden bending forward of the body with stiffening of the arms and legs or arching of the back while the arms and legs are extended. Infantile spasms rarely respond to the usual anti-seizure medications. Most children with infantile spasms have developmental disabilities later in life.

The guideline found that the hormone therapy adrenocorticotropic hormone, also known as ACTH, may be effective for treatment of infantile spasms. The seizure drug vigabatrin may also be considered for treatment, although evidence suggests ACTH may be more effective than vigabatrin. For children with seizures caused by the genetic disorder tuberous sclerosis complex, however, vigabatrin may be more effective.

The guideline, which is based on a review of all available evidence on treatment for infantile spasms and is an update of a guideline published in 2004, also found that low-dose ACTH is probably as effective as high-dose ACTH and it may lower the risk of side effects.

There is not enough evidence to know whether other treatments, alone or combined, are effective in treating infantile spasms, according to the guideline.

The guideline recommends that early diagnosis and early treatment may lead to better long-term outcomes for children’s development and learning skills.

"It is important for parents to talk to their child’s doctor if they suspect their child may be having seizures or spasms because early diagnosis and treatment may help in the long term with educational and learning skills," said guideline author Cristina Go, MD, of the Hospital for Sick Children in Toronto.

Go noted that children with the syndrome also have a specific pattern that shows up in tests of brain waves, and an EEG (electroencephalogram) is required for confirmation of the diagnosis.

Provided by American Academy of Neurology

Source: medicalxpress.com

June 10, 2012

The sight of unhealthy food during a period of sleep restriction activated reward centers in the brain that were less active when participants had adequate sleep, according to a new study using brain scans to better understand the link between sleep restriction and obesity.

Researchers from St. Luke’s – Roosevelt Hospital Center and Columbia University in New York performed functional magnetic resonance imaging (fMRI) on 25 men and women of normal weights while they looked at images of healthy and unhealthy foods. The scans were taken after five nights in which sleep was either restricted to four hours or allowed to continue up to nine hours. Results were compared.

"The same brain regions activated when unhealthy foods were presented were not involved when we presented healthy foods," said Marie-Pierre St-Onge, PhD, the study’s principal investigator. "The unhealthy food response was a neuronal pattern specific to restricted sleep. This may suggest greater propensity to succumb to unhealthy foods when one is sleep restricted."

Previous research has shown that restricted sleep leads to increased food consumption in healthy people, and that a self-reported desire for sweet and salty food increases after a period of sleep deprivation. St-Onge said the new study’s results provide additional support for a role of short sleep in appetite-modulation and obesity.

"The results suggest that, under restricted sleep, individuals will find unhealthy foods highly salient and rewarding, which may lead to greater consumption of those foods," St-Onge said. "Indeed, food intake data from this same study showed that participants ate more overall and consumed more fat after a period of sleep restriction compared to regular sleep. The brain imaging data provided the neurocognitive basis for those results.”

Provided by American Academy of Sleep Medicine

Source: medicalxpress.com

June 10, 2012

MRI scans from a study being presented today at SLEEP 2012 reveal how sleep deprivation impairs the higher-order regions in the human brain where food choices are made, possibly helping explain the link between sleep loss and obesity that previous research has uncovered.

Twenty-three healthy adults participated in two sessions using functional magnetic resonance imaging (fMRI), one after a normal night’s sleep and a second after a night of sleep deprivation. In both sessions, participants rated how much they wanted various food items shown to them while they were inside the scanner.

"Our goal was to see if specific regions of the brain associated with food processing were disrupted by sleep deprivation," said lead author Stephanie Greer, a graduate student at the Sleep and Neuroimaging Laboratory at the University of California, Berkeley.

Results show that sleep deprivation significantly impaired brain activity in the frontal lobe, a region critical for controlling behavior and making complex choices, such as the selection of food to eat. The study suggests that sleep loss may prevent the higher brain functions normally critical for making appropriate food choices, rather than necessarily changing activity in deeper brain structures that react to basic desire.

"We did not find significant differences following sleep deprivation in brain areas traditionally associated with basic reward reactivity,” Greer said. “Instead, it seems to be about the regions higher up in the brain, specifically within the frontal lobe, failing to integrate all the different signals that help us normally make wise choices about what we should eat.”

She added that this failure of the frontal lobe to optimally gather the information needed to decide on the right types of foods to eat – such as how healthy relative to how tasty an item may be – may represent one brain mechanism explaining the link between sleep loss and obesity.

"These results shed light on how the brain becomes impaired by sleep deprivation, leading to improper food choices," Greer said.

Provided by American Academy of Sleep Medicine

Source: medicalxpress.com

June 8, 2012

Molecular imbalance lies at the root of many psychiatric disorders. Current EU-funded research has discovered a major RNA molecular player in neurogenesis and has characterised its action and targets in the zebrafish embryo.

Credit: Thinkstock

Neural circuits are constantly in the process of modification according to experience and changes in the environment, a phenomenon known as plasticity. Classical Hebbian plasticity is crucial for encoding information whereas homeostatic plasticity stabilises neuronal activity in the face of changes that disturb excitability.

Homeostatic plasticity plays a big role in activity-dependent development of neural circuits. Interestingly, this type of homeostasis is frequently distorted in psychiatric disorders such as schizophrenia and autism.

Unlike the molecular basis of Hebbian homeostasis, the biochemistry behind homeostatic plasticity is relatively unknown. The ‘MicroRNAs and neurogenesis control’ (Neuromir) project set about investigating neural development in the zebrafish embryo to unravel the action of one class of gene regulator in particular – microRNAs.

The microRNA machinery is potentially very powerful in cell regulation. It influences many development processes and each microRNA molecule can regulate hundreds of target genes.

Numerous microRNAs are expressed in the development of the vertebrate central nervous system (CNS). Results from the in vivo study of the zebrafish revealed that miR-9 plays an important role in balancing the production of neurons during development of the embryo.

Neuromir researchers have successfully identified the molecular targets of miR-9. Future research may exploit this knowledge base by assessing their importance in disease and using their molecular format for drug therapy design.

Provided by CORDIS

Source: medicalxpress.com

June 8, 2012

Patients vary widely in their response to concussion, but scientists haven’t understood why. Now, using a new technique for analyzing data from brain imaging studies, researchers at Albert Einstein College of Medicine of Yeshiva University and Montefiore Medical Center have found that concussion victims have unique spatial patterns of brain abnormalities that change over time.

The new technique could eventually help in assessing concussion patients, predicting which head injuries are likely to have long-lasting neurological consequences, and evaluating the effectiveness of treatments, according to lead author Michael L. Lipton, M.D., Ph.D., associate director of the Gruss Magnetic Resonance Research Center at Einstein and medical director of magnetic resonance imaging (MRI) services at Montefiore. The findings are published today in the online edition of Brain Imaging and Behavior.

The Centers for Disease Control and Prevention estimates that more than one million Americans sustain a concussion (also known as mild traumatic brain injury, or mTBI) each year. Concussions in adults result mainly from motor vehicle accidents or falls. At least 300,000 adults and children are affected by sports-related concussions each year. While most people recover from concussions with no lasting ill effects, as many as 30 percent suffer permanent impairment – undergoing a personality change or being unable to plan an event. A 2003 federal study called concussions “a serious public health problem” that costs the U.S. an estimated $80 billion a year.

Previous imaging studies found differences between the brains of people who have suffered concussions and normal individuals. But those studies couldn’t assess whether concussion victims differ from one another. “In fact, most researchers have assumed that all people with concussions have abnormalities in the same brain regions,” said Dr. Lipton, who is also associate professor of radiology, of psychiatry and behavioral sciences, and in the Dominick P. Purpura Department of Neuroscience at Einstein. “But that doesn’t make sense, since it is more likely that different areas would be affected in each person because of differences in anatomy, vulnerability to injury and mechanism of injury.”

In the current study, the Einstein researchers used a recently developed MRI technique called diffusion tensor imaging (DTI) on 34 consecutive patients (19 women and 15 men aged 19 to 64) diagnosed with mTBI at Montefiore in the Bronx and on 30 healthy controls. The patients were imaged within two weeks of injury and again three and six months afterward.

The imaging data were then analyzed using a new software tool called Enhanced Z-score Microstructural Assessment Pathology (EZ-MAP), which allows researchers for the first time to examine microstructural abnormalities across the entire brain of individual patients. EZ-MAP was developed by Dr. Lipton and his colleagues at Einstein.

DTI detects subtle damage to the brain by measuring the direction of diffusion of water in white matter. The same technology was used by Dr. Lipton and his team in widely publicized research on more than 30 amateur soccer players who had all played the sport since childhood. They found that frequent headers showed brain injury similar to that seen in patients with concussion.

The uniformity of diffusion direction – an indicator of whether tissue has maintained its microstructural integrity – is measured on a zero-to-one scale called fractional anisotropy (FA). In the latest study, areas of abnormally low FA (reflecting abnormal brain regions) were observed in concussion patients but not in controls. Each concussion patient had a unique spatial pattern of low FA that evolved over the study period.

Surprisingly, each patient also had a unique, evolving pattern of abnormally high FA distinct from the areas of low FA. “We found widespread high FA at every time point, all the way out to six months and even in patients more than one year out from their injury.” said Dr. Lipton. “We suspect that high FA represents a response to the injury. In other words, the brain may be trying to compensate for the injury by developing and enhancing other neural connections. This is a new and unexpected finding.”

At present, diagnosis of concussions is based mainly on the nature of the patient’s accident and the presence of symptoms including headache, dizziness and behavioral abnormalities. DTI, combined with EZ-MAP analysis, might offer a more objective tool for diagnosing concussion injuries and for predicting which patients will have persistent and progressive symptoms.

Provided by Albert Einstein College of Medicine

Source: medicalxpress.com

ScienceDaily (June 7, 2012) — Using a new and powerful approach to understand the origins of neurodegenerative disorders such as Alzheimer’s disease, researchers at Mayo Clinic in Florida are building the case that these diseases are primarily caused by genes that are too active or not active enough, rather than by harmful gene mutations.

In the June 7 online issue of PLoS Genetics, they report that several hundred genes within almost 800 brain samples of patients with Alzheimer’s disease or other disorders had altered expression levels that did not result from neurodegeneration. Many of those variants were likely the cause.

"We now understand that disease likely develops from gene variants that have modest effects on gene expression, and which are also found in healthy people. But some of the variants — elevating expression of some genes, reducing levels of others — combine to produce a perfect storm that leads to dysfunction," says lead investigator Nilufer Ertekin-Taner, M.D., Ph.D., a Mayo Clinic neurologist and neuroscientist.

"If we can identify the genes linked to a disease that are too active or too dormant, we might be able to define new drug targets and therapies," she says. "That could be the case for both neurodegenerative disease as well as disease in general."

Dr. Ertekin-Taner says no other lab has performed the extent of brain gene expression study conducted at Mayo Clinic’s Florida campus. “The novelty, and the usefulness, of our study is the sheer number of brain samples that we looked at and the way in which we analyzed them. These results demonstrate the significant contribution of genetic factors that alter brain gene expression and increase risk of disease,” she says.

This form of data analysis measures gene expression levels by quantifying the amount of RNA produced in tissue and scans the genome of patients to identify genetic variants that associate with these levels.

Mayo researchers measured the level of 24,526 transcripts (messenger RNA) for 18,401 genes using cerebellar autopsy tissue from 197 Alzheimer’s disease patients and from 177 patients with other forms of neurodegeneration. The researchers then validated the results by examining the temporal cortex from 202 Alzheimer’s disease patients and from 197 with other pathologies. The difference between these samples is that while the temporal cortex is affected by Alzheimer’s disease, the cerebellum is relatively spared.

From these analyses, the researchers identified more than 2,000 markers of altered expression in both groups of patients that were common between the cerebellum and temporal cortex. Some of these markers also influenced risk of human diseases, suggesting their contribution to development of neurodegenerative and other diseases regardless of their location in the brain.

They identified novel expression “hits” for genetic risk markers of diseases that included progressive supranuclear palsy, Parkinson’s disease, and Paget’s disease, and confirmed other known associations for lupus, ulcerative colitis, and type 1 diabetes.

"Altered expression of brain genes can be linked to a number of diseases that affect the entire body," Dr. Ertekin-Taner says.

They then compared their eGWAS to GWAS data on Alzheimer’s disease, conducted by the federally funded Alzheimer’s Disease Genetics Consortium, to test whether some of the risk genes already identified promote disease through altered expression.

"We found that a number of genes already linked to Alzheimer’s disease do, in fact, have altered gene expression, but we also discovered that many of the variants in what we call the gray zone of the GWAS — genes whose contribution to Alzheimer’s disease was uncertain — were also influencing brain expression levels," Dr. Ertekin-Taner says. "That offers us new candidate risk genes to explore.

"This is a powerful approach to understanding disease," she says. "It can find new genes that contribute to risk, as well as new genetic pathways, and can also help us understand the function for a large number of genes and other molecular regulators in the genome that are implicated in very important diseases."

Source: Science Daily

ScienceDaily (June 7, 2012) — Degeneration of the axon and synapse, the slender projection through which neurons transmit electrical impulses to neighboring cells, is a hallmark of some of the most crippling neurodegenerative and brain diseases such as amyotrophic lateral sclerosis (ALS), Huntington’s disease and peripheral neuropathy. Scientists have worked for decades to understand axonal degeneration and its relation to these diseases. Now, researchers at the University of Massachusetts Medical School are the first to describe a gene — dSarm/Sarm1 — responsible for actively promoting axon destruction after injury. The research, published June 7 online by Science, provides evidence of an exciting new therapeutic target that could be used to delay or even stop axon decay.

"This discovery has the potential to have a profound impact on our understanding of neurodegenerative diseases, much like the discovery of apoptosis (programmed cell death) fundamentally changed our understanding of cancer," said Marc R. Freeman, PhD, associate professor of neurobiology at the University of Massachusetts Medical School and lead investigator on the study. "Identification of this gene allows us to start asking exciting new questions about the role of axon death in neurodegenerative diseases. For example, is it possible that these pathways are being inappropriately activated to cause premature axon death?"

For more than a century, scientists believed that injured axons severed from the neuron cell body passively wasted away due to a lack of nutrients. However, a mouse mutation identified in the early 1990s — called slow Wallerian degeneration (Wlds) — was able to suppress axon degeneration for weeks. This finding forced scientists to reassess Wallerian degeneration, the process through which an injured axon degenerates, as a passive process and consider the possibility that an active program of axon auto-destruction, akin to apoptotic death, was at work instead.

If Wallerian degeneration was an active process, hypothesized Dr. Freeman, a Howard Hughes Medical Institute Early Career Scientist, then it should be possible through forward genetic screens in Drosophila to identify mutants exhibiting Wlds-like axon protection. Freeman and colleagues screened more than 2,000 Drosophila mutants for ones that exhibited long-term survival of severed axons. Freeman says this was a heroic effort on the part of his colleagues. The screen took place over the next two and a half years, and involved seven students and post-docs in the Freeman lab — Jeannette M. Osterloh, A. Nicole Fox, PhD, Michelle A. Avery, PhD, Rachel Hackett, Mary A. Logan, PhD, Jennifer M. MacDonald, Jennifer S. Zeigenfuss — who performed the painstaking and labor-intensive experiments needed on each Drosophila mutant to identify flies that suppressed axonal degeneration after nerve injury.

Through these tests, they identified three mutants (out of the 2,000 screened) where severed axons survived for the lifespan of the fly. Next generation sequencing and chromosome deficiency mapping techniques were then used to isolate the single gene affected in all three — dSarm. These were loss-of-function alleles, meaning that Drosophila unable to produce the dSarm/Sarm1 molecule exhibited prolonged axon survival for as many as 30 days after injury. Freeman and colleagues went on to show that mice lacking Sarm1, the mammalian homolog of dSarm, also displayed remarkable preservation of injured axons. These findings provided the first direct evidence that Wallerian degeneration was driven by a conserved axonal death program and not a passive response to axon injury.

"For 20 years people have been looking for a gene whose normal function is to promote axon degeneration," said Osterloh, first author on the study. "Identification of the dSarm/Sarm1 gene has enormous therapeutic potential, for example as a knockdown target for patients suffering from diseases involving axonal loss."

The next step for Freeman and colleagues is to identify additional genes in the axon death pathway and investigate whether any have links with specific neurodegenerative diseases. “We’re already working with scientists at UMMS to understand the role axon death plays in ALS and Huntington’s disease,” said Freeman. “We are very excited about the possibility that these findings could have broad therapeutic potential in many neurodegenerative diseases.”

Source: Science Daily