Posts tagged neuroscience

Posts tagged neuroscience
Scientists have found a way of growing new blood vessels inside the body. They used cells derived from skin, that when injected into a damaged leg in massive numbers, moulded into the shape of a small blood vessel. This improved blood supply to withered muscles, giving them a new lease of life.
The technique, developed at King’s College London, could also be used to repair the damage done by heart attacks. Professor Qingbo Xu, who is funded by the British Heart Foundation, started by taking human skin cells. Using a cocktail of genes and chemicals, he turned them into early-stage blood vessel cells, programmed to form blood vessels.
He then injected half a million of these cells into the hind leg of a mouse whose foot muscles had been damaged due to poor circulation. These formed a small blood vessel that ferried blood to the damaged muscle, allowing it to repair itself, enabling the creature to put some weight on its foot, the journal Proceedings of the National Academy of Sciences reports.
The professor hopes that injected into the heart, the same cells could be used to heal damage done by heart attacks.
A condition believed to be a normal part of the ageing process has been found to have a negative effect on the brain function of older adults.
Leukoaraiosis, also known as small vessel ischemia, is a condition in which diseased blood vessels lead to small areas of damage in the white matter of the brain. The lesions are common in the brains of people over the age of 60, although the amount of disease varies among individuals.
"We know that aging is a risk factor for leukoaraiosis, and we suspect that high blood pressure may also play a role, … Different systems of the brain respond differently to disease, … White matter damage affects connections within the brain’s language network, which leads to an overall reduction in network activity." -Kirk M. Welker, M.D., assistant professor of radiology in the College of Medicine at Mayo Clinic in Rochester, Minn.
(Source: medicalxpress.com)
August 13, 2012
Researchers at Mount Sinai School of Medicine may have discovered why certain drugs to treat schizophrenia are ineffective in some patients. Published online in Nature Neuroscience, the research will pave the way for a new class of drugs to help treat this devastating mental illness, which impacts one percent of the world’s population, 30 percent of whom do not respond to currently available treatments.
A team of researchers at Mount Sinai School of Medicine set out to discover what epigenetic factors, or external factors that influence gene expression, are involved in this treatment-resistance to atypical antipsychotic drugs, the standard of care for schizophrenia. They discovered that, over time, an enzyme in the brains of schizophrenic patients analyzed at autopsy begins to compensate for the prolonged chemical changes caused by antipsychotics, resulting in reduced efficacy of the drugs.
"These results are groundbreaking because they show that drug resistance may be caused by the very medications prescribed to treat schizophrenia, when administered chronically," said Javier Gonzalez-Maeso, PhD, Assistant Professor of Psychiatry and Neurology at Mount Sinai School of Medicine and lead investigator on the study.
They found that an enzyme called HDAC2 was highly expressed in the brain of mice chronically treated with antipsychotic drugs, resulting in lower expression of the receptor called mGlu2, and a recurrence of psychotic symptoms. A similar finding was observed in the postmortem brains of schizophrenic patients. The research team administered a chemical called suberoylanilide hydroxamic acid (SAHA), which inhibits the entire family of HDACs. They found that this treatment prevented the detrimental effect of the antipsychotic called clozapine on mGlu2 expression, and also improved the therapeutic effects of atypical antipsychotics in mouse models.
Previous research conducted by the team showed that chronic treatment with the antipsychotic clozapine causes repression of mGlu2 expression in the frontal cortex of mice, a brain area key to cognition and perception. The researchers hypothesized that this effect of clozapine on mGlu2 may play a crucial role in restraining the therapeutic effects of antipsychotic drugs.
"We had previously found that chronic antipsychotic drug administration causes biochemical changes in the brain that may limit the therapeutic effects of these drugs,"said Dr. Gonzalez-Maeso. "We wanted to identify the molecular mechanism responsible for this biochemical change, and explore it as a new target for new drugs that enhance the therapeutic efficacy of antipsychotic drugs."
Mitsumasa Kurita, PhD, a postdoctoral fellow at Mount Sinai and the lead author of the study, said, “We found that atypical antipsychotic drugs trigger an increase of HDAC2 in frontal cortex of individuals with schizophrenia, which then reduces the presence of mGlu2, and thereby limits the efficacy of these drugs,” said
Dr. Gonzalez-Maeso’s team is now developing compounds that specifically inhibit HDAC2 as adjunctive treatments to antipsychotics. The study was funded by the National Institutes of Health.
Source: The Mount Sinai Hospital
The genetic code of the fruit fly Drosophila has been hacked into, allowing it to make proteins with properties that don’t exist in the natural world. The advance could ultimately lead to the creation of new or “improved” life forms in the burgeoning field of synthetic biology.
The four letters of the genetic code, A, C, T and G, are read in triplets, called codons, by the cell’s protein-making machinery. Each codon gives an instruction for the type of amino acid that gets added next in a protein chain, or tells the machinery to stop.
Complex proposition
As a proof of principle, Chin’s team has engineered fruit flies that incorporated three new amino acids into proteins in the cells of their ovaries.
The flies were engineered using bacteria that had been modified to insert the genetic code for the unnatural amino acid into the fly DNA. There was no apparent impact on the flies’ health, and they even produced healthy offspring that also made the new protein chains.
Bulletproof flies
None of the amino acids were particularly remarkable, but the fact that engineering the flies had no obvious impact on their health suggests that many more useful amino acids could be similarly incorporated.
For example, work in bacterial cells has shown that it is possible to incorporate unnatural amino acids that cross-link to each other or turn an enzyme’s activity on or off when a light is shone on them. Doing this in a complex organism like a fly could shed new light on how proteins interact within cells, or how rapidly turning an enzyme on or off affects the cell’s function.
The technique could even be used to create animals with new or improved properties, although that is probably some years off.
An Artificial Retina with the Capacity to Restore Normal Vision
Two researchers at Weill Cornell Medical College have deciphered a mouse’s retina’s neural code and coupled this information to a novel prosthetic device to restore sight to blind mice. The researchers say they have also cracked the code for a monkey retina — which is essentially identical to that of a human — and hope to quickly design and test a device that blind humans can use.
The breakthrough, reported in the Proceedings of the National Academy of Sciences (PNAS), signals a remarkable advance in longstanding efforts to restore vision. Current prosthetics provide blind users with spots and edges of light to help them navigate. This novel device provides the code to restore normal vision. The code is so accurate that it can allow facial features to be discerned and allow animals to track moving images.
(Image credit: Frank Müller, Institute of Complex Systems)

Dr Kristin Hillman and Professor David Bilkey have found that neurons in a specific region of the frontal cortex, called the anterior cingulate cortex, become active during decisions involving competitive effort.
The researchers have discovered that neurons in this region appear to store information on whether a course of action demands competition, what the intensity of that competition will be, and critically, whether or not the competition is ‘worth it’ to achieve an end reward.
Their study, which appears online in the journal Nature Neuroscience, is the first to examine how competitive behaviour is encoded by neurons in the brain.
Source: University of Otago
This is an abandoned and sealed science lab located in Moscow. The lab, which was operated by the Russian army, conducted sophisticated experiments studying human and animal brains.
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These days, 3D printing is being used to mock up far more complex systems, says Arthur Olson, who founded the molecular graphics lab at the Scripps Research Institute in La Jolla, California, 30 years ago. These include molecular environments made up of thousands of interacting proteins, which would be onerous-to-impossible to make any other way. With 3D printers, Olson says, “anybody can make a custom model”. But not everybody does: many researchers lack easy access to a printer, aren’t aware of the option or can’t afford the printouts (which can cost $100 or more).
Today, neuroscientists believe that your eye doesn’t see color at all — your brain creates it and constructs it through neural processes. Different features including color, shape, location, and velocity are picked up by different regions of the brain and then integrated into a holistic perception of an object.
Smelling a skunk after a cold: Brain changes after a stuffed nose protect the sense of smell
A new Northwestern Medicine study shows that after the human nose is experimentally blocked for one week, brain activity rapidly changes in olfactory brain regions. This change suggests the brain is compensating for the interruption of this vital sense. The brain activity returns to a normal pattern shortly after free breathing has been restored.
Previous research in animals has suggested that the olfactory system is resistant to perceptual changes following odor deprivation. This new paper focuses on humans to show how that’s possible. The study is published in the journal Nature Neuroscience.
"You need ongoing sensory input in order for your brain to update smell information," said Keng Nei Wu, the lead author of the paper and a graduate student in neuroscience at Northwestern University Feinberg School of Medicine. "When your nostrils are blocked up, your brain tries to adjust to the lack of information so the system doesn’t break down. The brain compensates for the lack of information so when you get your sense of smell back, it will be in good working order."