#First Contracting Human Muscle Grown in Laboratory Researchers at Duke university report the first lab-grown, contracting human muscle,
During culture, myobundles maintain functional acetylcholine receptors and structurally and functionally mature, evidenced by increased myofiber diameter and improved calcium handling and contractile strength.
the human spinal cord is able to trigger activity in the leg muscles using electrical pulses from an implanted stimulator.
Now, as part of a joint international project, a team of young researchers at the Center for Medical Physics and Biomedical engineering at Meduni Vienna has succeeded in identifying the mechanisms the spinal cord uses to control this muscle activity.
even if the neural pathways from the brain are interrupted physically as the result of a spinal cord injury.
Just like a set of building blocks, the neural network in the spinal cord is able to combine these basic patterns flexibly to suit the motor requirement,
The results have now been published in the leading journal rain Although the brain or brain stem acts as the command center,
it is the neural networks in the spinal cord that actually generate the complex motor patterns. These locomotion centers are to be found in most vertebrates.
when the spinal cord continues to transmit signals even when the brain is involved no longer, as in the headless chicken running around the farmyard.
Even after control by the brain has been lost, the spinal cord continues to send out motor signals, which are translated into movements of the legs and/or wings.
New possibilities for rehabilitation following spinal paralysis These new findings relating to the basic patterns for triggering
and coordinating muscle movements in the legs should also help in developing new approaches to rehabilitation aimed at utilizing those neural networks that are still functional following an accident
noninvasive method for stimulating the spinal cord, which involves attaching electrodes to the surface of the skin. his method allows easy access to the neural connections in the spinal cord below a spinal injury
and can therefore be offered to those suffering from paraplegia without exposing them to any particular medical risks
#Genetic Brain disorders Converge at the Synapse Several genetic disorders cause intellectual disability and autism. Historically, these genetic brain diseases were viewed as untreatable.
However, in recent years neuroscientists have shown in animal models that it is possible to reverse the debilitating effects of these gene mutations.
But the question remained whether different gene mutations disrupt common physiological processes. If this were the case,
In a paper published today in the online edition of Nature Neuroscience, a research team led by Mark Bear,
the Picower Professor of Neuroscience in MIT Picower Institute for Learning and Memory, showed that two very different genetic causes of autism
and intellectual disability disrupt protein synthesis at synapses, and that a treatment developed for one disease produced a cognitive benefit in the other.
called FMR1, is turned off during brain development. Fragile X is rare, affecting one in about 4, 000 individuals.
Bear and others discovered that the loss of this gene results in exaggerated protein synthesis at synapses, the specialized sites of communication between neurons.
Of particular interest, they found that this protein synthesis was stimulated by the neurotransmitter glutamate, downstream of a glutamate receptor called mglur5.
Some of the 27 affected genes play a role in protein synthesis regulation, leading Bear and colleagues to wonder if 16p11.2 microdeletion syndrome and fragile X syndrome affect synapses in the same way.
Synaptic protein synthesis was disrupted indeed in the hippocampus, a part of the brain important for memory formation.
similar to fragile X. Restoring brain function after disease onset These findings encouraged the MIT researchers to attempt to improve memory function in the 16p11.2 mice with the same approach that has worked in fragile X mice.
previously believed to be an intractable consequence of altered early brain development, might instead arise from ongoing alterations in synaptic signaling that can be corrected by drugs.
by removing a biochemical lampthat prevents connections between nerve cells in the brain from growing stronger.
The finding moves neuroscientists a step closer to figuring out how learning and memory work,
A report on the discovery appears Jan 7 in the journal Neuron. Animals learn and form memories
when connections called synapses among brain cells form and grow stronger. Researchers have known long that a crucial step in the process is the flow of calcium ions into the synapse area,
but hat happens next has been a mystery for 25 years, says Rick Huganir, Ph d.,director of the Solomon H. Snyder Department of Neuroscience at the Johns hopkins university School of medicine.
Previous studies suggested the calcium activates a protein called Camkii, but Camkii precise role in the process remained unknown.
added chemicals to lab-grown neurons to spur them to form stronger connections and saw that at rest,
a protein called Syngap was concentrated in so-called dendritic spines that form synapses with other cells a pattern previous experiments also had identified.
But once the synapse-strengthening process began Syngap flooded out of the dendritic spines. The spines then grew larger,
strengthening the synapses, Huganir says. The research team found that Syngap is clamped usually to the caffoldingthat gives dendritic spines their structure.
An influx of calcium into the synapse activates Camkii, which in turn unhooks Syngap from the cellsscaffolding
Compared to normal neurons, there was less Syngap in synapses when they were at rest, but activating Camkii did not noticeably change anything. his gives us a much clearer idea of how some Syngap mutations cause problems in the brain,
Huganir says. The findings may one day lead to drugs or other interventions that would lessen the effects of the mutations,
he says. Other authors on the paper are Menglong Zeng and Mingjie Zhang, both of Hong kong University of Science and Technology c
#Researchers Redefine Role of Brain's'Hunger Circuit'Using techniques developed only over the past few years,
UC San francisco researchers have completed experiments that overturn the scientific consensus on how the brain unger circuitgoverns eating.
Because of this circuit potential role in obesity, it has been studied extensively by neuroscientists and has attracted intense interest among pharmaceutical companies.
made up of two groups of cells known as Agrp and POMC neurons, senses long-term changes in the body hormone and nutrient levels,
and that the activation of Agrp neurons directly drives eating. But the new work shows that the Agrp-POMC circuit responds within seconds to the mere presence of food,
and that Agrp neurons motivate animals to seek and obtain food, rather than directly prompting them to consume it. o one would have predicted this.
what this region of the brain is doing. It has been known for 75 years that a region at the base of the brain called the hypothalamus exerts profound control over eating behavior.
As neuroscientists refined this observation over the ensuing decades, they zeroed in first on a small area of the hypothalamus known as the arcuate nucleus,
and more recently on Agrp and POMC neurons, two small populations of cells within that nucleus. These two groups of cells,
which collectively occupy an area smaller than a millimeter in the mouse brain, are organized functionally in a seesaw-like fashion:
when Agrp neurons are active, POMC neurons are not, and vice versa. Hundreds of experiments in which scientists added hormones or nutrients to brain slices
while recording the activity of Agrp and POMC neurons have laid the foundation of the dominant model of how the hunger circuit works.
As we grow hungry, this view holds, gradual changes in hormone levels send signals that begin to trigger Agrp neurons, the activity
of which eventually drives us to eat. As we become sated, circulating nutrients such as glucose activate POMC neurons,
which suppresses the desire to eat more food. Yiming Chen a graduate student in Knight lab, was expecting to build on the prevailing model of the hunger circuit
when he began experiments using newly developed fiber optic devices that allowed him to record Agrp-POMC activity in real time as mice were given food after a period of fasting. o one had recorded actually the activity of these neurons in a behaving mouse,
because the cells in this region are incredibly heterogeneous and located deep within the brain, said Chen. he technology to do this experiment has existed only for a few years.
But as reported in the February 19 2015 online issue of Cell, just seconds after food was given to the mice,
and before they had begun to eat, Chen saw Agrp activity begin to plummet, and POMC activity correspondingly begin to rise. ur prediction was that
if we gave a hungry mouse some food, then slowly, over many minutes, it would become satiated
and we would see these neurons slowly change their activity, Knight said. hat we found
almost immediately the neurons reversed their activation state. This happens when the mouse first sees
and Agrp neurons again beginning to fire, if the food were taken away. The magnitude of the transition from Agrp to POMC activity was correlated also directly with the palatability of the food offered:
while slow, hunger-induced changes in hormones and nutrients activate Agrp neurons over the long term,
these neurons are inactivated rapidly by the sight and smell of food alone. A major implication of this discovery
is that the function of Agrp neurons is to motivate hungry animals to seek and find food,
The fact that more accessible and more palatable, energy-rich foods engage POMC neurons and shut down Agrp activity more strongly suggests that the circuit also has nticipatoryaspects, by
which these neurons predict the nutritional value of a forthcoming meal and adjust their activity accordingly.
the most adaptive brain mechanism would suppress the motivation to continue searching; likewise, since energy-dense foods alleviate hunger for longer periods,
and the desire to seek additional nutrition. volution has made these neurons a key control point in the hunger circuit,
the Mcknight Foundation, the Alfred P. Sloan Foundation, a NARSAD Young Investigator Grant from the Brain and Behavior Research Foundation, the Esther A. and Joseph Klingenstein Foundation, the Program for Breakthrough
Dr. Maniatis is also a member of the Zuckerman Mind Brain Behavior Institute and director of Columbia university-wide precision medicine initiative. t now seems clear that future ALS treatments will not be equally effective for all patients because of the disease genetic diversity.
#New Brain Mapping Reveals Unknown Cell Types Using a process known as single cell sequencing, scientists at Karolinska Institutet have produced a detailed map of cortical cell types and the genes active within them.
and even managed to identify a number of hitherto unknown types. f you compare the brain to a fruit salad,
what colour juice you got from different parts of the brain, says Sten Linnarsson, senior researcher at the Department of Medical Biochemistry and Biophysics. ut in recent years wee developed much more sensitive methods of analysis that allow us to see which genes are active in individual cells.
especially as regards the brain, the body most complex organ. In the present study, the scientists used large-scale single-cell analysis to answer some of these questions.
By studying over three thousand cells from the cerebral cortex in mice, one at a time and in detail, and comparing which of the 20,000 genes were active in each one,
including a large proportion of specialised neurons, some blood vessel cells and glial cells, which take care of waste products,
protect against infection and supply nerve cells with nutrients. With the help of this detailed map, the scientists were able to identify hitherto unknown cell types,
including a nerve cell in the most superficial cortical layer, and six different types of oligodendrocyte,
which are cells that form the electrically insulating myelin sheath around the nerve cells. The new knowledge the project has generated can shed more light on diseases that affect the myelin
such as multiple sclerosis (MS). e could also confirm previous findings, such as that the pyramidal cells of the cerebral cortex are organised functionally in layers,
says Jens Hjerling-Leffler, who co-led the study with Dr Linnarsson. ut above all, we have created a much more detailed map of the cells of the brain that describes each cell type in detail
and shows which genes are active in it. This gives science a new tool for studying these cell types in disease models
and helps us to understand better how brain cell respond to disease and injury. There are estimated to be 100 million cells in a mouse brain
and 65 billion in a human brain. Nerve cells are approximately 20 micrometres in diameter, glial cells about 10 micrometres.
A micrometre is equivalent to a thousandth of a millimetre. The study was carried out by Sten Linnarsson and Jens Hjerling-Leffler research groups at the department of medical biochemistry and biophysics, in particular by Amit Zeisel and Ana Muños Manchado.
It also involved researchers from Karolinska Institutet Department of Oncology-Pathology, and Uppsala University. The study was financed with grants from several bodies,
including the European Research Council, the Swedish Research Council, the Swedish Cancer Society, the EU Seventh Framework Programme, the Swedish Society of Medicine, the Swedish Brain Fund, Karolinska Institutet strategic programme for neuroscience (Stratneuro), the Human Frontier Science Program
, the Åke Wiberg Foundation and the Clas Groschinsky Memorial Fund s
#Molecular Inhibitor Breaks Cycle That Leads to Alzheimer's A molecular chaperone has been found to inhibit a key stage in the development of Alzheimer disease and break the toxic chain reaction that leads to the death of brain cells, a new study shows.
The research provides an effective basis for searching for candidate molecules that could be used to treat the condition.
thereby helping to avoid the formation of highly toxic clusters that enable the condition to proliferate in the brain.
These oligomers are highly toxic to nerve cells and are thought now to be responsible for the devastating effects of Alzheimer disease.
The research team then carried out further tests in which living mouse brain tissue was exposed to amyloid-beta, the specific protein that forms the amyloid fibrils in Alzheimer disease.
but the toxicity did not develop in the brain tissue, confirming that the molecule had suppressed the chain reaction from secondary nucleation that feeds the catastrophic production of oligomers leading to Alzheimer disease.
and more likely to experience increased brain atrophy than non-carriers. his study demonstrates that tau deposits in the brains of Alzheimer disease subjects are not just a consequence of the disease,
said Anders M. Dale, Phd, professor of neurosciences and radiology and director of the Center for Translational Imaging and Precision Medicine at UC San diego and the study senior author e
#What Autism Can Teach Us About Brain Cancer Both disorders involve faults in the same protein.
Applying lessons learned from autism to brain cancer, researchers at The Johns hopkins university have discovered why elevated levels of the protein NHE9 add to the lethality of the most common and aggressive form of brain cancer, glioblastoma.
Their discovery suggests that drugs designed to target NHE9 could help to successfully fight the deadly disease.
for treating a deadly brain cancer says Rajini Rao, Ph d, . a professor of physiology at the Johns hopkins university School of medicine. his is a great example of the unexpected good that can come from going wherever the science takes us.
when placed on a surface mimicking that of the brain, suggesting a high potential for metastasis
or low NHE9, were transplanted into the brains of mice. This image is a drawing of a brain.
The overactive NHE9 protein is shown in blue over the brain. The argo carriers, or endosomes, of certain brain cancer cells contain overactive NHE9 proteins (blue),
which pump out too many protons (orange), changing the endosomesacidity and slowing their hipping speed.
Image credit: Hari Prasad and Rajini Rao. Based on their autism research, the team suspected that the boost NHE9 gave to glioblastomas was explained by abnormal endosome acidity.
NHE9 is overactive in brain cancer, causing endosomes to leak too many protons and become too alkaline.
and Extra Copies of Disease Gene in Alzheimer s Brain cells The surprise discovery offers a new understanding of Alzheimer s disease.
Scientists at The Scripps Research Institute (TSRI) have found diverse genomic changes in single neurons from the brains of Alzheimer s patients pointing to an unexpected factor that may underpin the most common form of the disease.
A new study published February 4 2015 in the online journal elife shows that Alzheimer s brains commonly have many neurons with significantly more DNA and genomic copies of the Alzheimer s-linked gene APP than normal brains.#
#Our findings open a new window into the normal and diseased brain by providing the first evidence that DNA variation in individual neurons could be related to brain function
and Alzheimer s disease#said Jerold Chun professor at TSRI and its Dorris Neuroscience Center and senior author of the new study.
Alzheimer s disease is an irreversible brain disease that tends to strike older people. It is progressive#impairing memory destroying motor skills and eventually causing death.
Researchers have known long about disease-related protein accumulations (called amyloid plaques) in the brains of Alzheimer s patients.
Chun and his laboratory group have had a longstanding interest in genomic variation among brain cells which produces#genomic mosaicism.#
#In 2001 Chun was the first to report that the brain contains many distinct genomes within its cells#much like the colorful tiles in an artist#s mosaic.#
#When we started genomic mosaicism in the brain was recognized not#said Chun.##But it turns out there is a remarkable range of genomic changes encompassed by DNA content variation in single brain cells.#
#In the new study Chun and his colleagues first set out to analyze the overall DNA content in cells comparing 32 postmortem Alzheimer s brains and 21 postmortem non-diseased brains.
Remarkably the researchers found that more than 90 percent of sporadic Alzheimer s disease brains displayed highly significant DNA increases of hundreds of millions more DNA base-pairs compared with control samples showing that genomic mosaicism was altered in the Alzheimer s brain.
Interestingly these changes were not found everywhere but were greatest in a part of the brain involved with complex thought.
Next the researchers used a technique called single-cell qpcr to determine the numbers of APP copies in 154 individual neurons from Alzheimer s and normal brains.
They also tested the neurons using a technique called FISH as an independent method to assess APP copies using fluorescent probes.
The researchers then quantified the copies of APP using both techniques. The tests showed that neurons from patients with sporadic Alzheimer s disease were four times as likely to contain more than the normal two copies of APP with some Alzheimer s neurons containing up to 12 copies of APP a phenomenon never seen in the controls.#
#A lot of people are still not aware of genomic mosaicism in the brain so to be able to connect it with a disease is really interesting#said Gwen Kaeser a graduate student studying in Chun#s lab and co-first author of the study with former graduate student Diane Bushman.
While genetic tests on blood samples can reveal if a person is prone to developing an inherited familial form of Alzheimer s most people who develop Alzheimer s do not test positive.
because the genomic signatures of sporadic Alzheimer s disease occur within individual brain cells. Indeed a majority of major brain diseases are also sporadic.
For example amyotrophic lateral sclerosis (ALS) can be linked to a gene in one to two percent of cases
Chun believes genomic mosaicism could possibly have a role in other brain diseases. Future studies in the Chun lab will investigate the relationship between mosaicism
and disease the causes of mosaicism and potential new disease drug targets present in the millions of extra base-pairs found in single Alzheimer s disease neurons.
In addition to Chun Kaeser and Bushman other authors of the study#Genomic mosaicism with increased amyloid precursor protein (APP) gene copy number in single neurons from sporadic Alzheimer s disease brains#were Jurgen
Full open access research for#Genomic mosaicism with increased amyloid precursor protein (APP) gene copy number in single neurons from sporadic Alzheimer s disease brains#by Diane M Bushman
#Previous reports have shown that individual neurons of the brain can display somatic genomic mosaicism of unknown function.
In this study we report altered genomic mosaicism in single sporadic Alzheimer s disease (AD) neurons characterized by increases in DNA content and amyloid precursor protein (APP) gene copy number.
Two independent single-cell copy number analyses identified amplifications at the APP locus. The use of single-cell qpcr identified up to 12 copies of APP in sampled neurons.
These data identify somatic genomic changes in single neurons affecting known and unknown loci which are increased in sporadic AD
#Researchers Enlarge Brain Samples Making Them Easier to Image New technique enables nanoscale-resolution microscopy of large biological specimens.
says Ed Boyden, an associate professor of biological engineering and brain and cognitive sciences at MIT. Boyden is the senior author of a paper describing the new method in the Jan 15 online edition of Science.
who is a member of MIT Media Lab and Mcgovern Institute for Brain Research. Protein complexes, molecules that transport payloads in and out of cells,
and take a long time to image large samples. f you want to map the brain, or understand how cancer cells are organized in a metastasizing tumor,
the MIT team was able to image a section of brain tissue 500 by 200 by 100 microns with a standard confocal microscope.
MIT researchers led by Ed Boyden have invented a new way to visualize the nanoscale structure of the brain and other tissues.
The researchers envision that this technology could be very useful to scientists trying to image brain cells
Boyden says. specially for the brain, you have to be able to image a large volume of tissue,
While Boyden team is focused on the brain, other possible applications for this technique include studying tumor metastasis
It Thync, a wearable device that zaps your brain with low levels of pulsed electrical energy to calm you down
who has a Ph d. in neuroscience and bioengineering and Isy Goldwasser, is a wireless device that pairs with an iphone
Zap Your Brain To Change Your Mood Shanklin describes the calm mode giving him a feeling
The energy mode provide his brain with more clarity. Thync is considered a lifestyle product, as opposed to a medical device,
#Needle Injects Healing Electronics into the Brain Researchers have built a tiny mesh-like electronic sensor,
and injected it into the brain. The device taking this fantastic electronic voyage may soon be able to zap tumors,
repair damaged spinal cords or even connect parts of the brain like an artificial synapse. The key finding is that the sensor
and mesh combination is so small and bendy that it doesn cause any damage to the surrounding brain tissue, something that often plagues surgical procedures done with a needle, knife or other type of probe.
Could A Brain Implant Cure Depression? f one is thinking of trying to change the way one does long term brain implants,
it could be a really big deal, said Charles Lieber, chemistry professor at Harvard university and lead author on the new paper published in the journal Nature Nanotechnology. ou can promote a positive interaction
After an injection several centimeters into the brain of a laboratory mouse the scientists were able to monitor electronic brain signals.
Zhenan Bao, professor of chemical engineering at Stanford university who is also building injectable electronics, said the experiment was n amazing piece of work. he concept is said ingenious,
Brain-Zapping Implant Could Aid Injured Soldiers The authors of the paper say next step is to use the mesh system to deliver living stem cells that may help repair damaged sections of the brain or perhaps a multifunction electronic device
#'Wi-fi'Nanoparticles Send Signals from the Brain The problem with talking to our own brains,
The brain uses complex electrical fields and impulses to move information around on the atomic level.
A medical research team at Florida International University in Miami injected 20 billion nanoparticles into the brains of mice
with the idea of establishing a kind of direct wireless connection to neurons. DNEWS: Brain-To-Brain Networking Takes First Baby Stepsthe agnetoelectricnanoparticles (MENS) injected in the mice have several special properties.
First, theye small enough to sidle up to the neural network itself. Within whispering distance, you might say.
Secondly, the particles can be triggered by an outside magnetic field to produce an electric field when adjacent to individual neurons.
should be able to communicate directly with the brain electric field. hen MENS are exposed to even an extremely low frequency magnetic field,
the electric field can directly couple to the electric circuitry of the neural network. he nanoparticles could be used to deliver drugs to specific parts of the brain.
Wearable device Changes Your Moodthe technique could also be used to create a new kind of brain-computer interface.
the nanoparticles could generate measurable magnetic fields in response to the brain electrical fields. Toggle the system back
but due to an ill-advised rey Anatomybinge-watching incident last night, my brain and I are not currently on speaking terms. via New Scientis k
#Brain-Sensing Headband Helps Users Manage Stress Technology and relaxation don always go hand in hand. However, a brain-sensing headband that reads brain waves
and provides real-time feedback has been developed to help users better focus and manage stress. The Muse headband is lined with seven EEG sensors that detect the brain electrical activity
and sends information about the user state of mind to a smartphone app, Calm, which is available on both ios and Android.
Interaxon, the company behind the Muse headband and a Mars venture client, claims that sustained use of the device will train one brain to stay more naturally calm and focused.
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