Neuroscience
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Most people know the frustration of having a word on the “tip of your tongue” that they simply can’t remember. But that passing nuisance can be an everyday occurrence for someone with aphasia, a communication disorder caused by a stroke or other brain damage that impairs the ability to process language.
About 1 million Americans — roughly one in every 250 — are affected by aphasia, which can also impact reading and writing skills. But how they acquire the problem and how long they’ll endure it differ from person to person, explained Ellayne Ganzfried, a speech-language pathologist and executive director of the National Aphasia Association.
"No two people with aphasia are alike because everyone’s brain responds to the injury in a different way," Ganzfried said. "About half of people who have aphasia recover quickly, within the first few days. If the symptoms of aphasia last longer than two or three months, a complete recovery is unlikely … [though] some people continue to improve over a period of years and even decades."
Strokes are the most common cause, followed by head injuries, tumors, migraines or other neurological issues. Depending on the damage to the brain regions controlling language, which are typically in the left hemisphere, the resulting aphasia can be broken into four broad categories:
"Processing language requires the collaboration of lots of different parts or systems of the brain," explained Karen Riedel, director of speech-language pathology at the Rusk Institute of Rehabilitation Medicine at NYU Langone Medical Center in New York City. "The whole brain ‘talks’ — the whole brain has something to do with the use of language."
Because of this, a variety of therapies are used to help people regain as much speech and language as possible. But regardless of the injury, people with aphasia have the best chances for recovery when language therapy begins immediately, Riedel said.
Because aphasia is so variable, a therapy that helps one person might not help another, she noted. Tried-and-true techniques include melodic intonation therapy, which uses melody and rhythm to help improve the ability to retrieve words, and constraint-induced therapy, which forces people to use speech over other communication methods.
But technology, Riedel said, has introduced new language-improvement techniques into the mix over the last few years that are both exciting and fun. Several apps available for iPhone or iPad involve synthetic speech that helps engage those with aphasia in yet another realm of communication.
"Our patients have much more access to different kinds of programs that are computer-based," she said. "There’s always something new around the corner."
What remains a constant concern, however, is the misunderstanding many people have of those with language difficulties and how to treat them, Ganzfried and Riedel agreed.
"Many people with aphasia will become socially isolated because of their communication difficulties, which can lead to depression," Ganzfried said. "There are also many misconceptions about aphasia, including that the person is mentally unstable or under the influence of drugs or alcohol. It’s also extremely frustrating. Imagine knowing what you want to say in your head but you can’t get the words out."
Researchers at Brigham and Women’s Hospital have found that melatonin supplementation significantly improved sleep in hypertensive patients taking beta-blockers
Over 20 million people in the United States take beta-blockers, a medication commonly prescribed for cardiovascular issues, anxiety, hypertension and more. Many of these same people also have trouble sleeping, a side effect possibly related to the fact that these medications suppress night-time melatonin production. Researchers at Brigham and Women’s Hospital (BWH) have found that melatonin supplementation significantly improved sleep in hypertensive patients taking beta-blockers.
The study will be electronically published on September 28, 2012 and will be published in the October print issue of SLEEP (Title: A mechanism for upper airway stability during slow wave sleep).
"Beta-blockers have long been associated with sleep disturbances, yet until now, there have been no clinical studies that tested whether melatonin supplementation can improve sleep in these patients," explained Frank Scheer, PhD, MSc, an associate neuroscientist at BWH, and principal investigator on this study. "We found that melatonin supplements significantly improved sleep."
The research team analyzed 16 hypertensive patients who regularly took beta-blockers as treatment for their hypertension. The study participants were given either a melatonin supplement or placebo to take each night before bed. To avoid bias, neither the participants nor the researchers knew which pill they were taking. During the three week study, the participants spent two separate four-day visits in lab. While in the lab, the researchers assessed the participants’ sleep patterns and found a 37-minute increase in the amount of sleep in the participants who received the melatonin supplement compared to those who received placebo. They also found an eight percent improvement of sleep efficiency and a 41 minute increase in the time spent in Stage 2 sleep, without a decrease in slow wave sleep or REM sleep.
"Over the course of three weeks, none of the study participants taking the melatonin showed any of the adverse effects that are often observed with other, classic sleep aids. There were also no signs of ‘rebound insomnia’ after the participants stopped taking the drug," explained Scheer, who is also an assistant professor of Medicine at Harvard Medical School. "In fact, melatonin had a positive carry-over effect on sleep even after the participants had stopped taking the drug."
The researchers caution that while this data is promising for hypertensive patients taking beta-blockers, more research is needed to determine whether patients taking beta-blockers for causes other than hypertension could also benefit from melatonin supplementation.
In what could be a breakthrough in the treatment of deadly brain tumors, a team of researchers from Barrow Neurological Institute and Arizona State University has discovered that the immune system reacts differently to different types of brain tissue, shedding light on why cancerous brain tumors are so difficult to treat.
The large, two-part study, led by Barrow research fellow Sergiy Kushchayev, MD under the guidance of Dr. Mark Preul, Director of Neurosurgery Research, was published in the Sept. 14 issue of Cancer Management and Research
The study explores the effects of immunotherapy on malignant gliomas, cancerous brain tumors that typically have a poor prognosis.
What the researchers discovered was that immune cells of the brain and of the blood exhibit massive rearrangements when interacting with a malignant glioma under treatment. Essentially, the study demonstrates that the complex immune system reacts differently in different brain tissues and different regions of the brain, including tumors.
"This is the first time that researchers have conducted a regional tissue study of the brain and a malignant glioma to show that these immune cells do not aggregate or behave in the same way in their respective areas of the brain," says Dr. Preul. "This means that effective treatment in one area of the brain may not be effective in another area. In fact, it could even cause other regions of the tumor to become worse."
The results of the study provide important insight into why clinical trials involving immunotherapies on glioma patients may not be working.
Scientists may be one step closer to predicting the uncertain course of relapsing-remitting multiple sclerosis (MS), a disease that can lay dormant for months or years, thanks to the discovery of a unique genetic marker. The marker, detailed by researchers in the August edition of The Journal of Immunology, is the first of its kind to be directly linked to MS.
The study, supported by funding from both the National Institutes of Health (NIH) and the Ohio State Center for Clinical and Translational Science (CCTS) was conducted by a team of scientists with The Ohio State University using blood samples from patients with MS, as well as mouse models. Researchers uncovered the molecule miR-29, while working to identify a biomarker in the blood that could indicate if a patient had an ongoing inflammatory response, such as MS.
“Our research was inspired by the knowledge gap that existed between microRNA and MS, as well as the unpredictable nature of MS,” said Kristen Smith, Ph.D., principal investigator, who received a “mentorship grant” to conduct the study alongside senior scientists at The Ohio State University Wexner Medical Center. “By identifying a unique marker associated with MS, we hope to inspire a relatively noninvasive test that could identify and predict the course of the disease, helping clinicians tailor therapies to disease progression.”
Source: newswise
Different anti-aging treatments work together and add years of life
The combination of two neuroprotective therapies, voluntary physical exercise, and the daily intake of melatonin has been shown to have a synergistic effect against brain deterioration in rodents with three different mutations of Alzheimer’s disease.
A study carried out by a group of researchers from the Barcelona Biomedical Research Institute (IIBB), in collaboration with the University of Granada and the Autonomous University of Barcelona, shows the combined effect of neuroprotective therapies against Alzheimer’s in mice.
Daily voluntary exercise and daily intake of melatonin, both of which are known for the effects they have in regulating circadian rhythm, show a synergistic effect against brain deterioration in the 3xTg-AD mouse, which has three mutations of Alzheimer’s disease.
"For years we have known that the combination of different anti-aging therapies such as physical exercise, a Mediterranean diet, and not smoking adds years to one’s life," Coral Sanfeliu, from the IIBB, explains to SINC. "Now it seems that melatonin, the sleep hormone, also has important anti-aging effects".
The experts analysed the combined effect of sport and melatonin in 3xTg-AD mice which were experiencing an initial phase of Alzheimer’s and presented learning difficulties and changes in behaviour such as anxiety and apathy.
The mice were divided into one control group and three other groups which would undergo different treatments: exercise –unrestricted use of a running wheel–, melatonin –a dose equivalent to 10 mg per kg of body weight–, and a combination of melatonin and voluntary physical exercise. In addition, a reference group of mice were included which presented no mutations of the disease.
"After six months, the state of the mice undergoing treatment was closer to that of the mice with no mutations than to their own initial pathological state. From this we can say that the disease has significantly regressed," Sanfeliu states.
The results, which were published in the journal Neurobiology of Aging, show a general improvement in behaviour, learning, and memory with the three treatments.
These procedures also protected the brain tissue from oxidative stress and provided good levels of protection from excesses of amyloid beta peptide and hyperphosphorylated TAU protein caused by the mutations. In the case of the mitochondria, the combined effect resulted in an increase in the analysed indicators of improved performance which were not observed independently.
Mice with brittle skin, which tears off in order to escape predators, may offer clues to healing wounds without scarring, according to US researchers.
Some African spiny mice lost up to 60% of the skin from their backs, says the study published in the journal Nature. Unlike wounds in other mammals, the skin then rapidly healed and regrew hairs rather than forming a scar. Scientists want to figure out how the healing takes place and if it could apply to people.
Salamanders, some of which can regrow entire limbs, are famed for their regenerative abilities. It has made them the focus of many researchers hoping to figure out how to produce the same effect in people. Mammals, however, have very limited ability to regrow lost organs. Normally a scar forms to seal the wound. “This study shows that mammals as a group may in fact have higher regenerative abilities then they are given credit for,” said Dr Ashley Seifert from the University of Florida.
An evolutionary biologist at The University of Manchester, working with scientists in the United States, has found compelling evidence that parts of the brain can evolve independently from each other. It’s hoped the findings will significantly advance our understanding of the brain.
The unique 15-year study with researchers at the University of Tennessee and Harvard Medical School also identified several genetic loci that control the size of different brain parts.
The aim of the research was to find out if different parts of the brain can respond independently of each other to evolutionary stimulus (mosaic evolution) or whether the brain responds as a whole (concerted evolution). Unlike previous studies the researchers compared the brain measurements within just one species. The findings have been published in the journal Nature Communications.
The brains of approximately 10,000 mice were analysed. Seven individual parts of each brain were measured by volume and weight. The entire genome, except the Y chromosome, was scanned for each animal and the gene set for each brain part identified.
Dr Reinmar Hager from the Faculty of Life Sciences compared variation in the size of the brain parts to variation in the genes. He found that the variation in the size of brain parts is controlled by the specific gene set for that brain part and not a shared set of genes.
He also compared the measurements for each mouse to the overall size of its brain. Surprisingly he found very little correlation between the sizes of the brain parts and the overall size of the brain.
Dr Hager says: “If all the different brain parts evolved as a whole we would expect that the same set of genes influences size in all parts. However, we found many gene variations for each different part of the brain supporting a mosaic scenario of brain evolution. We also found very little correlation between the size of the brain parts and the overall size of the brain. This again supports the mosaic evolutionary hypothesis.”
Using the data collected from the mice Dr Hager and colleagues analysed the genes that influence the size of the brain to the genes that control the size of the body. They wanted to find out how independent size regulation of the brain is to that of the body.
They found evidence that the size of the brain is governed by an independent gene set to the one that controls the size of the body. Again they found vey little correlation between variations in the size of the body and the brain.
The evidence means that overall brain size can evolve independently of body size.
Following this research more work will be carried out to identify the specific genes that underlie the size of different parts in the brain
Dr Hager says: “If we can identify the specific genes that cause variations in the size of brain parts then there will be big implications for researchers looking at neuronal disease and brain development. We hope this research will significantly advance our understanding of the brain.”
Brain metastases are common secondary complications of other types of cancer, particularly lung, breast and skin cancer. The body’s own immune response in the brain is rendered powerless in the fight against these metastases by inflammatory reactions. Researchers at the MedUni Vienna have now, for the first time, precisely characterised the brain’s immune response to infiltrating metastases. This could pave the way to the development of new, less aggressive treatment options.
“The active phagocytes are quite literally overwhelmed by the tumour and even the white blood cells are too weak to fight off these metastases on their own; they have to be stimulated before they can have any effect,” explains oncologist Matthias Preusser from the University Department of Internal Medicine I and the Comprehensive Cancer Center (CCC), a joint institution operated by the MedUni Vienna and the Vienna General Hospital.
Brain tissue was obtained for investigation from autopsies carried out on people who had metastatic disease secondary to breast, lung or skin cancer. These are also the most common types of primary tumour. Brain metastases develop because they spread from the tumours into other parts of the body right up to the brain.
The scientists at the Clinical Institute of Neurology, the Centre for Brain Research, the CCC and the University Department of Internal Medicine I have discovered that metastases in the brain do encounter a wall of phagocytes, but it is too weak to successfully arrest the tumour’s development. To do this, white blood cells (lymphocytes) need to be mobilised in greater numbers as the second instance of the immune defence system.
These findings could lead to new therapeutic strategies being developed that will aim to increase the activation of white blood cells or other parts of the immune system – perhaps through medication such as antibody treatments or vaccines.
300 to 400 patients with brain metastases are treated each year at the MedUni Vienna. The standard treatment in most cases is radiotherapy to the head or generalised irradiation of the brain – which is associated with certain risks and possible side effects. Only in very few cases are drug-based treatment methods available for certain types of cancer. Says Preusser: “Our findings could represent an important step towards the development of less aggressive forms of treatment.”
The hippocampus represents an important brain structure for learning. Scientists at the Max Planck Institute of Psychiatry in Munich discovered how it filters electrical neuronal signals through an input and output control, thus regulating learning and memory processes. Accordingly, effective signal transmission needs so-called theta-frequency impulses of the cerebral cortex. With a frequency of three to eight hertz, these impulses generate waves of electrical activity that propagate through the hippocampus. Impulses of a different frequency evoke no transmission, or only a much weaker one. Moreover, signal transmission in other areas of the brain through long-term potentiation (LTP), which is essential for learning, occurs only when the activity waves take place for a certain while. The scientists even have an explanation for why we are mentally more productive after drinking a cup of coffee or in an acute stress situation: in their experiments, caffeine and the stress hormone corticosterone boosted the activity flow.
UCI study points to role endocannabinoids play in common genetic cause of autism
American and European scientists have found that increasing natural marijuana-like chemicals in the brain can help correct behavioral issues related to fragile X syndrome, the most common known genetic cause of autism.
The work indicates potential treatments for anxiety and cognitive defects in people with this condition. Results appear online in Nature Communications.
Daniele Piomelli of UC Irvine and Olivier Manzoni of INSERM, the French national research agency, led the study, which identified compounds that inhibit enzymes blocking endocannabinoid transmitters called 2-AG in the striatum and cortex regions of the brain.
These transmitters allow for the efficient transport of electrical signals at synapses, structures through which information passes between neurons. In fragile X syndrome, regional synapse communication is severely limited, giving rise to certain cognitive and behavioral problems.
Fragile X syndrome is caused by a mutation of the FMR1 gene on the X chromosome. People born with it are mentally disabled; generally experience crawling, walking and language delays; tend to avoid eye contact; may be hyperactive or impulsive; and have such notable physical characteristics as an elongated face, flat feet and large ears.
The researchers stress that their findings, while promising, do not point to a cure for the condition.
“What we hope is to one day increase the ability of people with fragile X syndrome to socialize and engage in normal cognitive functions,” said Piomelli, a UCI professor of anatomy & neurobiology and the Louise Turner Arnold Chair in the Neurosciences.
The study involved mice genetically altered with FMR1 mutations that exhibited symptoms of fragile X syndrome. Treated with novel compounds that correct 2-AG protein signaling in brain cells, these mice showed dramatic behavioral improvements in maze tests measuring anxiety and open-space acceptance.
While other work has focused on pharmacological treatments for behavioral issues associated with fragile X syndrome, Piomelli noted that this is the first to identify the role endocannabinoids play in the neurobiology of the condition.
About endocannabinoids
Endocannabinoid compounds are created naturally in the body and share a similar chemical structure with THC, the primary psychoactive component of the marijuana plant, Cannabis. Endocannabinoids are distinctive because they link with protein molecule receptors — called cannabinoid receptors — on the surface of cells. For instance, when a person smokes marijuana, the cannabinoid THC activates these receptors. Because the body’s natural cannabinoids control a variety of factors — such as pain, mood and appetite — they’re attractive targets for drug discovery and development. Piomelli is one of the world’s leading endocannabinoid researchers. His groundbreaking work is showing that this system can be exploited by new treatments to combat anxiety, pain, depression and obesity.