Posts tagged neuroscience
Articles and news from the latest research reports.
Robots are everywhere. But for them to be useful, they have to be programmed by people. Computer scientists are now looking for ways to teach robots how to teach themselves.
Goldilocks was on to something when she preferred everything “just right.” Harvard Medical School researchers have found that when it comes to the length of mitochondria, the power-producing organelles, applying the fairy tale’s mantra is crucial to the health of a cell. More specifically, abnormalities in mitochondrial length promote the development of neurodegenerative diseases such as Alzheimer’s.
"There had been a fair amount of interest in mitochondria in Alzheimer’s and tau-related diseases, but causality was unknown," said Brian DuBoff, first author of the study and a post-doctoral research fellow at Massachusetts General Hospital.
"Ultimately, a deeper understanding of the relationship between mitochondrial function and Alzheimer’s may guide us to develop more targeted therapies in the future," said Mel Feany, HMS professor of pathology at Brigham and Women’s Hospital and senior author of the paper.
The findings were published online in the August 23 issue of Neuron.
New research funded primarily by the Department of Defense would help emergency care workers and battlefield medics stabilize blood flow in the brains of traumatic injury victims. Rice University and Baylor College of Medicine in Houston developed a nanoparticle-based antioxidant that quickly quenches free radicals that interfere with regulation of the brain’s vascular system.
Imagine if we could understand the language two neurons use to communicate. We might learn something about how thoughts and consciousness are formed. At the very least, our improved understanding of neuron communication would help biologists study the brain with more precision than ever before.
Heather Clark, an associate professor of pharmaceutical sciences at Northeastern University, has received a $300,000 Young Faculty Award from the Defense Advanced Research Projects Agency to explore neural cell communication using her expertise in nanosensors.
Therapeutic Avenues for Parkinson’s Investigated
ScienceDaily (Aug. 23, 2012) — Scientists at the University of Houston (UH) have discovered what may possibly be a key ingredient in the fight against Parkinson’s disease.
Affecting more than 500,000 people in the U.S., Parkinson’s disease is a degenerative disorder of the central nervous system marked by a loss of certain nerve cells in the brain, causing a lack of dopamine. These dopamine-producing neurons are in a section of the midbrain that regulates body control and movement. In a study recently published in the Proceedings of the National Academy of Sciences (PNAS), researchers from the UH Center for Nuclear Receptors and Cell Signaling (CNRCS) demonstrated that the nuclear receptor liver X receptor beta (LXRbeta) may play a role in the prevention and treatment of this progressive neurodegenerative disease.
"LXRbeta performs an important function in the development of the central nervous system, and our work indicates that the presence of LXRbeta promotes the survival of dopaminergic neurons, which are the main source of dopamine in the central nervous system," said CNRCS director and professor Jan-Åke Gustafsson, whose lab discovered LXRbeta in 1995. "The receptor continues to show promise as a potential therapeutic target for this disease, as well as other neurological disorders."
To better understand the relationship between LXRbeta and Parkinson’s disease, the team worked with a potent neurotoxin, called MPTP, a contaminant found in street drugs that caused Parkinson’s in people who consumed these drugs. In lab settings, MPTP is used in murine models to simulate the disease and to study its pathology and possible treatments.
The researchers found that the absence of LXRbeta increased the harmful effects of MPTP on dopamine-producing neurons. Additionally, they found that using a drug that activates LXRbeta receptors prevented the destructive effects of MPTP and, therefore, may offer protection against the neurodegeneration of the midbrain.
"LXRbeta is not expressed in the dopamine-producing neurons, but instead in the microglia surrounding the neurons," Gustafsson said. "Microglia are the police of the brain, keeping things in order. In Parkinson’s disease the microglia are overactive and begin to destroy the healthy neurons in the neighborhood of those neurons damaged by MPTP. LXRbeta calms down the microglia and prevents collateral damage. Thus, we have discovered a novel therapeutic target for treatment of Parkinson’s disease."
Source: Science Daily
Squid Skin Dances When You Blast Cypress Hill At It
The music causes a current to flow in wires hooked up to a squid, exciting its tissue. The video here shows an 8x microscope zoomed on the the dorsal side of the caudal fin of the Longfin Inshore Squid, which produces three colors in its process: brown, red, and yellow.
DNA detectives track down nerve disorder cause
Better diagnosis and treatment of a crippling inherited nerve disorder may be just around the corner thanks to an international team that spanned Asia, Europe and the United States. The team had been hunting DNA strands for the cause of the inherited nerve disorder known as spinocerebellar ataxia, or SCA. The disease causes progressive loss of balance, muscle control and ability to walk. Thanks to their diligence and detective work they have discovered the disease gene in a region of chromosome 1 where another group from the Netherlands had previously shown linkage with a form of SCA called SCA19, and the Taiwanese group on the new paper had shown similar linkage in a family for a form of the disease that was then called SCA22. The international team, from France, Japan, Taiwan and the USA have published their discovery in the Annals of Neurology. The Dutch group has also published results in the same issue of the journal.
Their paper reveals that mutations in the gene KCND3 were found in six families in Asia, Europe and the United States that have been haunted by SCA. Their results will allow for a better understanding of why nerves in the brain’s movement-controlling centre die, and how new DNA mapping techniques can find the causes of other diseases that run in families.
Margit Burmeister, Ph.D., a geneticist at University of Michigan Health System (U-M), helped lead the work and stressed that the gene could not have been found without a great deal of DNA detective work and the cooperation of the families who volunteered to let researchers map all the DNA of multiple members of their family tree. ‘We combined traditional genetic linkage analysis in families with inherited diseases with whole exome sequencing of an individual’s DNA, allowing us to narrow down and ultimately identify the mutation,’ she says. ‘This new type of approach has already resulted in many new gene identifications, and will bring in many more.’
The gene is very important as it manages the production of a protein that allows nerve cells to ‘talk’ to one another through the flow of potassium. Pinpointing its role as a cause of ataxia will now allow more people with ataxia to learn the exact cause of their disease, give a very specific target for new treatments, and perhaps allow the families to stop the disease from affecting future generations.
U-M neurologist Vikram Shakkottai, M.D., Ph.D., an ataxia specialist and co-author on the paper, also notes that the new genetic information will help patients find out the specific cause of their disease. He and his colleagues are already working to find drugs that might alter potassium flow, and provide a treatment for a group of diseases that currently are only treated with supportive care such as physical activity and balance training as patients deteriorate. ‘Many of the families who come to our clinic for treatment don’t have a recognised genetic mutation, so it’s important to find new genetic mutations to explain their symptoms,’ says Shakkottai. ‘But at the same time, this research is helping us understand a common mechanism of nerve cell dysfunction in progressive and non-progressive disease.’
Their findings however are not restricted to just ataxia. The researchers were also able to show that when KCND3 is mutated, it causes poor communication between nerve cells in the cerebellum as well as the death of those cells. This discovery could aid research on other neurological disorders involving balance and movement.
The Dutch team, that also published its findings about KCND3 at the same time, studied families in the Netherlands and found that mutations on the gene are responsible for SCA19, the cause of which had up until now been a mystery. ‘In other words, mutations in this gene are not uncommon and present all over the world,’ says Burmeister. ‘This means that in the future, this gene should be tested for mutations as part of a clinical genetic test panel for patients with ataxia symptoms. Because a generation can be skipped, it may even be relevant in some sporadic cases - those where the patient isn’t aware of any other family members with a similar disease.’
Source: Cordis News
Helium reveals gibbon’s soprano skill
Apes are unlikely to become virtuosos at the opera house, but gibbons have naturally mastered some of the vocal techniques that human sopranos rely on, scientists in Japan report.
The research shows that, like humans, gibbons use a ‘source–filter’ mode of sound generation. The sound originates from the creatures’ vocal folds as a mixture of different harmonics, which are multiples of the frequency at which the vocal folds vibrate. The resonant frequencies of the vocal tract then determine which of these harmonics are projected. By altering the position of the mouth, lips and teeth, humans vary these resonant frequencies to make the different sounds required for speech.
The gibbon’s melodious calling bears many similarities to the techniques of human singers. Like professional sopranos, gibbons tune the resonant frequency of their vocal tract to the pitch frequency generated by the vocal folds to amplify the sound. Acoustic physicist Joe Wolfe of the University of New South Wales in Sydney, Australia, says that this type of “resonance tuning” is something that comes fairly easily to human singers and is key to their ability to project their voice over a loud orchestra.
Elucidating the neural pathways that underlie brain function is one of the greatest challenges in neuroscience. Light sheet based microscopy is a cutting edge method to map cerebral circuitry through optical sectioning of cleared mouse brains. However, the image contrast provided by this method is not sufficient to resolve and reconstruct the entire neuronal network. Here we combined the advantages of light sheet illumination and confocal slit detection to increase the image contrast in real time, with a frame rate of 10 Hz. In fact, in confocal light sheet microscopy (CLSM), the out-of-focus and scattered light is filtered out before detection, without multiple acquisitions or any post-processing of the acquired data. The background rejection capabilities of CLSM were validated in cleared mouse brains by comparison with a structured illumination approach. We show that CLSM allows reconstructing macroscopic brain volumes with sub-cellular resolution. We obtained a comprehensive map of Purkinje cells in the cerebellum of L7-GFP transgenic mice. Further, we were able to trace neuronal projections across brain of thy1-GFP-M transgenic mice. The whole-brain high-resolution fluorescence imaging assured by CLSM may represent a powerful tool to navigate the brain through neuronal pathways. Although this work is focused on brain imaging, the macro-scale high-resolution tomographies affordable with CLSM are ideally suited to explore, at micron-scale resolution, the anatomy of different specimens like murine organs, embryos or flies.
Scientists find switch in the brain that could cause psychosis and addiction for cannabis users
(Source: Daily Mail)