Neuroscience
Month
Measurements of five protein biomarkers in the cerebrospinal fluid helped to differentiate Alzheimer’s disease from Parkinson’s disease with dementia and from dementia with Lewy bodies in a cross-sectional study of individuals at Swedish neurology and memory disorder clinics.
The diagnostic accuracy of this panel of tests in distinguishing Alzheimer’s disease from dementia with Lewy bodies “is at least in the same order of magnitude as that obtained with dopamine transporter imaging, and with a lower cost,” Dr. Sara Hall of the department of clinical sciences, Lund (Sweden) University, Malmö, and her associates wrote in a study published Aug. 27 in Archives of Neurology.
In addition, one of the five biomarkers in this panel appears to differentiate Parkinson’s disease from atypical parkinsonism such as that seen in progressive supranuclear palsy, multiple system atrophy, or corticobasal degeneration, the researchers noted.
Their results confirmed those of previous studies postulating that CSF total tau (T-tau) and phophorylated tau (P-tau) levels are higher in Alzheimer’s than in the other two dementias, whereas amyloid-beta (Abeta) 1-42 levels are lower in Alzheimer’s than in the other two dementias.
Columbia neurophysiologist David Sulzer took his first piano lessons at the age of 11 and was playing his violin and guitar in bars by age 15. Later he gained a national following as a founder of the Soldier String Quartet and the Thai Elephant Orchestra—an actual orchestra of elephants in northern Thailand—and for playing with the likes of Bo Diddley, the Velvet Underground’s John Cale and the jazz great Tony Williams.
From left, Brad Garton and David Sulzer discuss turning brain waves into music on WHYY/PBS in Philadelphia.
It was only after arriving at Columbia, however, that the musician-turned-research-scientist embarked on perhaps his most exotic musical venture—using a computer to translate the spontaneous patterns of his brain waves into music.
With the help of Brad Garton, director of Columbia’s Computer Music Center, Sulzer has performed his avant-garde brain wave music in solo recitals and with musical ensembles.
Last spring, Sulzer presented a piece entitled Reading Stephen Colbert at a conference in New York City sponsored by Columbia and the Paris-based IRCAM (Institut de Recherche et Coordination Acoustique/Musique), a global center of musical research.
Sulzer, a professor in the departments of Psychiatry, Neurology and Pharmacology, wore electrodes attached to his scalp to measure voltage fluctuations in his brain as he sat in a chair reading a book by the comedian. Those fluctuations were fed into a computer program created by Garton, which transformed them into musical notes.
Are you a morning lark or a night owl? Scientists use that simplified categorization to explain that different people have different internal body clocks, commonly called circadian clocks. Sleep-wake cycles, digestive activities, and many other physiological processes are controlled by these clocks. In recent years, researchers have found that internal body clocks can also affect how patients react to drugs. For example, timing a course of chemotherapy to the internal body time of cancer patients can improve treatment efficacy and reduce side effects.
Round the clock. Tracking the levels of 50 hormones and amino acids in blood samples (shown by ribbons) reveals a body’s internal time. Credit: PNAS
But physicians have not been able to exploit these findings because determining internal body time is, well, time consuming. It’s also cumbersome. The most established and reliable method requires taking blood samples from a patient hourly and tracking levels of the hormone melatonin, which previous research has tied closely to internal body time.
Now a Japanese group has come up with an alternative method of determining internal body time by constructing what it calls a molecular timetable based on levels in blood samples of more than 50 metabolites—hormones and amino acids—that result from biological activity. The researchers established a molecular timetable based on samples from three subjects and validated it using the conventional melatonin measurement. They then used that timetable to determine the internal body times of other subjects by checking the levels of the metabolites in just two blood samples from each subject per day.
Having such a timetable could allow doctors to synchronize drug delivery to internal body time, the team reports online today in the Proceedings of the National Academy of Sciences. “Usually personalized medicine is focusing on genetic differences, but there are also temporal differences [among patients]. That will be the next step in personalized medicine,” says systems biologist Hiroki Ueda of the RIKEN Center for Developmental Biology in Kobe, Japan, who heads the research group.
"In principle, the method holds great promise as a way of replacing the cumbersome melatonin assay," says Steven Brown, a molecular biologist at the University of Zurich in Switzerland. "The authors show in a small-scale, well-controlled experiment that they are able to predict internal body time within a precision frame of 3 hours," says Urs Albrecht of the University of Fribourg in Switzerland. Both researchers say further work will be necessary to make the technique more practical and more widely applicable, and Ueda agrees. The experimental subjects were all young men, and different molecular timetables are likely needed for women and for people of different ages. He would also like to improve the precision and make it reliable with just one blood sample per day.
Source: ScienceNOW
ScienceDaily (Aug. 27, 2012) — Muscular dystrophy is a complicated set of genetic diseases in which genetic mutations affect the various proteins that contribute to a complex that is required for a structural bridge between muscle cells and the extracellular matrix (ECM) that provides the physical and chemical environment required for their development and function.
The affects of these genetic mutations in patients vary widely, even when the same gene is affected. In order to develop treatments for this disease, it is important to have an animal model that accurately reflects the course of the disease in humans. In this issue of the Journal of Clinical Investigation, researchers at the University of Iowa report the development of a mouse model of Fukuyama’s muscular dystrophy that copies the pathology seen in the human form of the disease.
By removing the gene fukutin from mouse embryos at various points during development, researchers led by Kevin Campbell were able to determine that fukutin disrupts important modifications of dystrophin that prevent the muscle cells from attaching to the ECM. Disruption of the gene earlier in development led to a more severe form of the disease, suggesting that fukutin is important for muscle maturation. Disruptions in later stages of development caused a less severe form of the disease. In a companion piece, Elizabeth McNally of the University of Chicago discusses the implications of this disease model for the development of new therapies to treat muscular dystrophy.
Source: Science Daily
August 26, 2012
Vitamin B12 is essential to human health. However, some people have inherited conditions that leave them unable to process vitamin B12. As a result they are prone to serious health problems, including developmental delay, psychosis, stroke and dementia. An international research team recently discovered a new genetic disease related to vitamin B12 deficiency by identifying a gene that is vital to the transport of vitamin into the cells of the body. This discovery will help doctors better diagnose this rare genetic disorder and open the door to new treatments. The findings are published in the journal Nature Genetics.
"We found that a second transport protein was involved in the uptake of the vitamin into the cells, thus providing evidence of another cause of hereditary vitamin B12 deficiency", said Dr. David Rosenblatt, one of the study’s co-authors, scientist in medical genetics and genomics at the Research Institute of the McGill University Health Centre (RI MUHC) and Dodd Q. Chu and Family Chair in Medical Genetics and the Chair of the Department of Human Genetics at McGill University. "It is also the first description of a new genetic disease associated with how vitamin B12 is handled by the body".
These results build on previous research by the same team from the RI MUHC and McGill University, with their colleagues in Switzerland, Germany and the United States. In previous work, the researchers discovered that vitamin B12 enters our cells with help from of a specific transport protein. In this study, they were working independently with two patients showing symptoms of the cblF gene defect of vitamin B12 metabolism but without an actual defect in this gene. Their work led to the discovery of a new gene, ABCD4, associated with the transport of B12 and responsible for a new disease called cblJ combined homocystinuria and methylmalonic aciduria (cblJ-Hcy-MMA).
Using next generation sequencing of the patients’ genetic information, the scientists identified two mutations in the same ABCD4 gene, in both patients. “We were also able to compensate for the genetic mutation by adding an intact ABCD4 protein to the patients’ cells, thus allowing the vitamin to be properly integrated into the cells,” explained Dr. Matthias Baumgartner, senior author of the study and a Professor of metabolic diseases at Zurich’s University Children’s Hospital.
Vitamin B12, or cobalamin, is essential for healthy functioning of the human nervous system and red blood cell synthesis. Unable to produce the vitamin itself, the human body has to obtain it from animal-based foods such as milk products, eggs, red meat, chicken, fish, and shellfish – or vitamin supplements. Vitamin B12 is not found in vegetables.
"This discovery will lead to the early diagnosis of this serious genetic disorder and has given us new paths to explore treatment options. It also helps explain how vitamin B12 functions in the body, even for those without the disorder," said Dr. Rosenblatt who is the director of one of only two referral laboratories in the world for patients suspected of having this genetic inability to absorb vitamin B12. Dr. Rosenblatt points out that the study of patients with rare diseases is essential to the advancement of our knowledge of human biology.
Source: medicalxpress.com
26 August 2012 by Mo Costandi
Subjects trained to sniff pleasant smells while asleep retain the conditioning when they wake up.
It sounds like every student’s dream: research published today in Nature Neuroscience shows that we can learn entirely new information while we snooze.
TIPS/Photoshot
Anat Arzi of the Weizmann Institute of Science in Rehovot, Israel, and her colleagues used a simple form of learning called classical conditioning to teach 55 healthy participants to associate odours with sounds as they slept.
They repeatedly exposed the sleeping participants to pleasant odours, such as deodorant and shampoo, and unpleasant odours such as rotting fish and meat, and played a specific sound to accompany each scent.
It is well known that sleep has an important role in strengthening existing memories, and this conditioning was already known to alter sniffing behaviour in people who are awake. The subjects sniff strongly when they hear a tone associated with a pleasant smell, but only weakly in response to a tone associated with an unpleasant one.
But the latest research shows that the sleep conditioning persists even after they wake up, causing them to sniff strongly or weakly on hearing the relevant tone — even if there was no odour. The participants were completely unaware that they had learned the relationship between smells and sounds. The effect was seen regardless of when the conditioning was done during the sleep cycle. However, the sniffing responses were slightly more pronounced in those participants who learned the association during the rapid eye movement (REM) stage, which typically occurs during the second half of a night’s sleep.
Pillow power
Arzi thinks that we could probably learn more complex information while we sleep. “This does not imply that you can place your homework under the pillow and know it in the morning,” she says. “There will be clear limits on what we can learn in sleep, but I speculate that they will be beyond what we have demonstrated.”
In 2009, Tristan Bekinschtein, a neuroscientist at the UK Medical Research Council’s Cognition and Brain Sciences Unit in Cambridge, and his colleagues reported that some patients who are minimally conscious or in a vegetative state can be classically conditioned to blink in response to air puffed into their eyes. Conditioned responses such as these could eventually help clinicians to diagnose these neurological conditions, and to predict which patients might subsequently recover. “It remains to be seen if the neural networks involved in sleep learning are similar to the ones recruited during wakefulness,” says Bekinschtein.
The findings by Arzi and her colleagues might also be useful for these purposes, and could lead to ‘sleep therapies’ that help to alter behaviour in conditions such as phobia.
“We are now trying to implement helpful behavioural modification through sleep-learning,” says Arzi. “We also want to investigate the brain mechanisms involved, and the type of learning we use in other states of altered consciousness, such as vegetative state and coma.”
Source: Nature
The nervous system is a complex collection of nerves and specialized cells known as neurons that transmit signals between different parts of the body. Vertebrates — animals with backbones and spinal columns — have central and peripheral nervous systems.
The central nervous system is made up of the brain, spinal cord and retina. The peripheral nervous system consists of sensory neurons, ganglia (clusters of neurons) and nerves that connect to one another and to the central nervous system.
Credit: iDesign, Shutterstock
Description of the nervous system
The nervous system is essentially the body’s electrical wiring. It is composed of nerves, which are cylindrical bundles of fibers that start at the brain and central cord and branch out to every other part of the body.
Neurons send signals to other cells through thin fibers called axons, which cause chemicals known as neurotransmitters to be released at junctions called synapses. A synapse gives a command to the cell and the entire communication process typically takes only a fraction of a millisecond.
Sensory neurons react to physical stimuli such as light, sound and touch and send feedback to the central nervous system about the body’s surrounding environment. Motor neurons, located in the central nervous system or in peripheral ganglia, transmit signals to activate the muscles or glands.
Glial cells, derived from the Greek word for “glue,” support the neurons and hold them in place. Glial cells also feed nutrients to neurons, destroy pathogens, remove dead neurons and act as traffic cops by directing the axons of neurons to their targets. Specific types of glial cells (oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system) generate layers of a fatty substance called myelin that wraps around axons and provides electrical insulation to enable them to rapidly and efficiently transmit signals.
24 August 2012 by Michael Marshall
THE latest twist in the origin-of-life tale is double helical. Chemists are close to demonstrating that the building blocks of DNA can form spontaneously from chemicals thought to be present on the primordial Earth. If they succeed, their work would suggest that DNA could have predated the birth of life.
Lurking at the dawn of time (Image: Snorri Gunnarsson/Flickr/Getty)
DNA is essential to almost all life on Earth, yet most biologists think that life began with RNA. Just like DNA, it stores genetic information. What’s more, RNA can fold into complex shapes that can clamp onto other molecules and speed up chemical reactions, just like a protein, and it is structurally simpler than DNA, so might be easier to make.
After decades of trying, in 2009 researchers finally managed to generate RNA using chemicals that probably existed on the early Earth. Matthew Powner, now at University College London, and his colleagues synthesised two of the four nucleotides that make up RNA. Their achievement suggested that RNA may have formed spontaneously - powerful support for the idea that life began in an “RNA world”.
August 24th, 2012
Researchers from the Laboratory of astrocyte biology and CNS regeneration headed by Prof. Milos Pekny just published a research article in a prestigious journal Stem Cells on the molecular mechanism that controls generation of new neurons in the brain.
Astrocytes are cells that have many functions in the central nervous system, such as the control of neuronal synapses, blood flow, or the brain’s response to neurotrauma or stroke.
Reduces brain tissue damage
Prof. Pekny’s laboratory together with collaborators have earlier demonstrated that astrocytes reduce the brain tissue damage after stroke and that the integration of transplanted neural stem cells can be largely improved by modulating the activity of astrocytes.
Generation of new neurons
In their current study, the Sahlgrenska Academy researchers show how astrocytes control the generation of new neurons in the brain. An important contribution to this project came from Åbo Academy, one of Sahlgrenska’s traditional collaborative partners.
“In the brain, astrocytes control how many new neurons are formed from neural stem cells and survive to integrate into the existing neuronal networks. Astrocytes do this by secreting specific molecules but also by much less understood direct cell-cell interactions with stem cells”, says Prof. Milos Pekny.
Image shows GFAP stained cortex from a TgAPP mouse showing activated astrocytes from a different study.
Important regulator
“Astrocytes are in physical contact with neural stem cells and we have shown that they signal through the Notch pathway to stem cells to keep the birth rate of new neurons low. We have also shown that the intermediate filament system of astrocytes is an important regulator of this process. It seems that astrocyte intermediate filaments can be used as a target to increase the birthrate of new neurons.”
Target for future therapies
“We are starting to understand some of the cellular and molecular mechanisms behind the control of neurogenesis. Neurogenesis is one of the components of brain plasticity, which plays a role in the learning process as well as in the recovery after brain injury or stroke. This work helps us to understand how plasticity and regenerative response can be therapeutically promoted in the future”, says Prof. Milos Pekny.
Source: Neuroscience News
The researchers from Lancaster University have found that those with the degenerative brain disease have difficulty with one particular test. They also found that the inability to carry out the tests in those who had already been diagnosed with Alzheimer’s was linked to lower memory function.
Photo: ALAMY
Dr Trevor Crawford said the latest results were potentially exciting. They showed, for the first time, a physical connection with the memory impairment that so often is the first noticeable symptom in Alzheimer’s.
Dr Crawford, of the department of Psychology and the Centre for Ageing Research, Lancaster University, said: “The diagnosis of Alzheimer’s disease is currently heavily dependent on the results of a series of lengthy neuropsychological tests.
"However, patients with a dementia often find that these tests are difficult to complete due to a lack of clear understanding and lapse in their attention or motivation.
"Over the last 10 years, researchers in laboratories around the world have been working on an alternative approach based on the brain’s control of the movements of the eye as a tool for investigating cognitive abilities, such as attention, cognitive inhibition and memory."
During the study, 18 patients with Alzheimer’s disease, 25 patients with Parkinson’s disease, 17 healthy young people and 18 healthy older people were asked to follow the movements of light on a computer monitor. In some instances they were asked to look away from the light. Detailed eye–tracking measurements showed stark contrasts in results.
Patients with Alzheimer’s made errors on the task when they were asked to look away from the light. They were unable correct those errors, despite being able to respond normally when they were asked to look towards the light.
These uncorrected errors were 10 times more frequent in the Alzheimers’ patients than the control groups. Researchers also measured memory function among those Alzheimer’s patients who found the test difficult and were able to show a clear correlation with lower memory function. Dr Crawford added: “The light tracking test could play a vital role in the diagnosis of Alzheimer’s.”
August 24, 2012 By Barbara Bronson Gray
(HealthDay)—Whether it’s an email from an unknown gentleman on another continent pleading for money or a financial scammer selling a promising penny stock, the young and old tend to be more easily duped than middle-aged people.
Changes in this region could explain why seniors, children are less doubting.
Now, researchers have pinpointed the area of the brain responsible for this gullibility and have theorized why it makes children, teens and seniors less likely to doubt.
The ventromedial area of the prefrontal cortex of the brain—a softball-sized lobe in the front of your head, just above your eyes—appears to be responsible for allowing you to pause after hearing or reading something and consider whether it’s true, according to a study published recently in the journal Frontiers in Neuroscience.
ScienceDaily (Aug. 23, 2012) — We use language every day to express our emotions, but can this language actually affect what and how we feel? Two new studies from Psychological Science, a journal of the Association for Psychological Science, explore the ways in which the interaction between language and emotion influences our well-being.
Putting Feelings into Words Can Help Us Cope with Scary Situations
Katharina Kircanski and colleagues at the University of California, Los Angeles investigated whether verbalizing a current emotional experience, even when that experience is negative, might be an effective method for treating for people with spider phobias. In an exposure therapy study, participants were split into different experimental groups and they were instructed to approach a spider over several consecutive days.
One group was told to put their feelings into words by describing their negative emotions about approaching the spider. Another group was asked to ‘reappraise’ the situation by describing the spider using emotionally neutral words. A third group was told to talk about an unrelated topic (things in their home) and a fourth group received no intervention. Participants who put their negative feelings into words were most effective at lowering their levels of physiological arousal. They were also slightly more willing to approach the spider. The findings suggest that talking about your feelings — even if they’re negative — may help you to cope with a scary situation.
Unlocking Past Emotion: The Verbs We Use Can Affect Mood and Happiness
Our memory for events is influenced by the language we use. When we talk about a past occurrence, we can describe it as ongoing (I was running) or already completed (I ran). To investigate whether using these different wordings might affect our mood and overall happiness, Will Hart of the University of Alabama conducted four experiments in which participants either recalled or experienced a positive, negative, or neutral event. They found that people who described a positive event with words that suggested it was ongoing felt more positive. And when they described a negative event in the same way, they felt more negative.
The authors conclude that one potential way to improve mood could be to talk about negative past events as something that already happened as opposed to something that was happening.
Source: Science Daily