A new study shows that newborns that have been exposed to nicotine from both active and passive smoking mothers show poor physiological, sensory, motor and attention responses.
"Newborns who have had intrauterine exposure to nicotine, whether in an active or passive way, show signs of being more affected in terms of their neurobehavioural development. This could be an indicator of pathologies, independently of sociodemographic, obstetric and paediatric factors," as explained to SINC by Josefa Canals and Carmen Hernández, the lead authors of the study.
Filed under passive smoking nicotine exposure cognition brain neuroscience psychology science
Using ultrasound waves, MIT engineers have found a way to enhance the permeability of skin to drugs, making transdermal drug delivery more efficient. This technology could pave the way for noninvasive drug delivery or needle-free vaccinations, according to the researchers.
“This could be used for topical drugs such as steroids — cortisol, for example — systemic drugs and proteins such as insulin, as well as antigens for vaccination, among many other things,” says Carl Schoellhammer, an MIT graduate student in chemical engineering and one of the lead authors of a recent paper on the new system.
Ultrasound — sound waves with frequencies greater than the upper limit of human hearing — can increase skin permeability by lightly wearing away the top layer of the skin, an effect that is transient and pain-free.
In a paper appearing in the Journal of Controlled Release, the research team found that applying two separate beams of ultrasound waves — one of low frequency and one of high frequency — can uniformly boost permeability across a region of skin more rapidly than using a single beam of ultrasound waves.
Filed under transdermal drug delivery drug delivery insulin ultrasound skin transdermal health neuroscience science
The most common form of strokes are caused by a sudden reduction in blood flow to the brain (ischemia) that leads to an inadequate supply of oxygen and nutrients. These so-called ischemic strokes are one of the leading causes of death and disability in industrialized nations. If they are not immediately remedied by medical intervention, areas of the brain may die off. In the journal Angewandte Chemie, Korean researchers have now proposed a new approach for supplemental treatment: Ceria nanoparticles could trap the reactive oxygen compounds that result from ischemia and cause cells to die.
Filed under ceria nanoparticles ischemia ischemic stroke stroke oxygen cells cell death neuroscience brain science
A drug designed for diabetes sufferers could have the potential to treat neurodegenerative diseases like Alzheimer’s, a study by scientists at the University of Ulster has revealed.
Type II diabetes is a known risk factor for Alzheimer’s and it is thought that impaired insulin signalling in the brain could damage nerve cells and contribute to the disease.
Scientists believe that drugs designed to tackle Type II diabetes could also have benefits for keeping our brain cells healthy.
To investigate this, Prof Christian Hölscher and his team at the Biomedical Sciences Research Institute on the Coleraine campus used an experimental drug called (Val8)GLP-1.
This drug simulates the activity of a protein called GLP-1, which can help the body control its response to blood sugar. The scientists treated healthy mice with the drug and studied its effects in the brain.
Although it is often difficult for drugs to cross from the blood into the brain, the team found that (Val8)GLP-1 entered the brain and appeared to have no side-effects at the doses tested.
The drug promoted new brain cells to grow in the hippocampus, an area of the brain known to be involved in memory. This finding suggests that as well as its role in insulin signalling, GLP-1 may also be important for the production of new nerve cells in the mouse brain.
The team found that blocking the effect of GLP-1 in the brain made mice perform more poorly on learning and memory task, while boosting it with the drug seemed to have no effect on behaviour.
The new findings, published this week in the journal Brain Research, are part of ongoing research funded by Alzheimer’s Research UK, the leading dementia research charity.
Prof Hölscher, said: “Here at the Biomedical Sciences Research Institute, we are really interested in the potential of diabetes drugs for protecting brain cells from damage and even promoting new brain cells to grow. This could have huge implications for diseases like Alzheimer’s or Parkinson’s, where brain cells are lost.
“It is very encouraging that the experimental drug we tested, (Val8)GLP-1, entered the brain and our work suggests that GLP-1 could be a really important target for boosting memory. While we didn’t see benefits on learning and memory in these healthy mice, we are keen to test the drugs in mice with signs of Alzheimer’s disease, where we could see real improvements.”
Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said: “We are pleased to have supported this early stage research, suggesting that this experimental diabetes drug could also promote the growth of new brain cells. While we know losing brain cells is a key feature of Alzheimer’s, there is a long way to go before we would know whether this drug could benefit people with the disease.
"This research will help us understand the factors that keep nerve cells healthy, knowledge that could hold vital clues to tackling Alzheimer’s. With over half a million people in the UK living with the disease, learning more about how to keep our brain cells healthy is of vital importance. Funding for dementia research lags far behind that of other common diseases, but is essential if we are to realise the true potential of research like this.”
(Source: alphagalileo.org)
Filed under alzheimer alzheimer's disease diabetes type II diabetes protein GLP-1 (Val8)GLP-1 drug
Nanoengineers at the University of California, San Diego have developed a novel technology that can fabricate, in mere seconds, microscale three dimensional (3D) structures out of soft, biocompatible hydrogels. Near term, the technology could lead to better systems for growing and studying cells, including stem cells, in the laboratory. Long-term, the goal is to be able to print biological tissues for regenerative medicine. For example, in the future, doctors may repair the damage caused by heart attack by replacing it with tissue that rolled off of a printer.
The biofabrication technique uses a computer projection system and precisely controlled micromirrors to shine light on a selected area of a solution containing photo-sensitive biopolymers and cells. This photo-induced solidification process forms one layer of solid structure at a time, but in a continuous fashion.
Filed under biofabrication technique brain cells neuroscience stem cells technology tissue science
Surgery Has a More Profound Effect than Anesthesia on Brain Pathology and Cognition in Alzheimer’s Animal Model, Finds Penn Study
A syndrome called “post-operative cognitive decline” has been coined to refer to the commonly reported loss of cognitive abilities, usually in older adults, in the days to weeks after surgery. In fact, some patients time the onset of their Alzheimer’s disease symptoms from a surgical procedure. Exactly how the trio of anesthesia, surgery, and dementia interact is clinically inconclusive, yet of great concern to patients, their families and physicians.
A year ago, researchers at the Perelman School of Medicine at the University of Pennsylvania reported that Alzheimer’s pathology, as reflected by cerebral spinal fluid biomarkers, might be increased in patients after surgery and anesthesia. However, it is not clear whether the anesthetic drugs or the surgical procedure itself was responsible. To separate these possibilities, the group turned to a mouse model of Alzheimer’s disease.
The results, published online this month in the Annals of Surgery, show that surgery itself, rather than anesthesia, has the more profound impact on a dementia-vulnerable brain.
Filed under post-operative cognitive decline alzheimer alzheimer's disease surgery anesthesia neuroscience brain science
Mark Mallman plans to create music for seven straight days and nights by wiring himself up to sensors that translate his brain waves into music around the clock.
(Source: wired.co.uk)
Filed under brainwaves brain brain activity music technology marathon IV mark mallman neuroscience science
During the 1980s, thousands of infants in Romanian orphanages spent up to 20 hours a day lying untouched in their cribs, deprived of human contact. As they grew up, neurological and psychological tests confirmed a haunting phenomenon observed in other species, such as mice and rhesus monkeys: Early isolation and neglect can produce lasting cognitive damage, ranging from severe emotional instability to mental retardation. Now, researchers say they have discovered a possible explanation for why early neglect wreaks such havoc—isolation may stunt the growth of the brain cells that insulate neurons, resulting in slower communication between different areas of the brain.
Scientists have known for 50 years that the strength and arrangement of connections between neurons changes as we learn and experience new things, says Gabriel Corfas, senior author of the paper published online today in Science and a neuroscientist at Harvard Medical School in Boston and Boston Children’s Hospital. But the role of the brain’s non-neuronal cells in creating, strengthening, and shaping these neural circuits is more mysterious. The brain’s “white matter”—as opposed to its gray matter, which is composed of neurons—consists mostly of glial cells, which produce the fat and protein myelin sheaths that insulate a neuron’s branching axons, the slender fibers that conduct electrical impulses to other cells. One purpose of myelin, scientists think, is to reduce “leakage” of electric current as electrochemical signals zip to and fro. When the myelin is thin or damaged, the signals can’t travel as fast; that slowdown can impair many different brain functions, including motor control, language, and memory.
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Filed under brain cognitive impairment social deprivation social isolation neuroscience neuron psychology science
In a study published in The American Naturalist, a group of scientists led by the Zoological Society of London (ZSL) have used a technique developed to study human consumer choices to investigate what influences a baboon’s foraging decisions. The technique, known as discrete choice modelling, has rarely been used before in animal behaviour research. It showed how baboons not only consider many social and non-social factors when making foraging decisions, but also how they change these factors depending on their habitat and their own social traits.
Filed under animals primates foraging discrete choice modelling animal behavior neuroscience science
Signs of autism—such as impaired social skills and repetitive, ritualistic movements—usually begin to appear when a child is about 18 months old. Autism is thought to result from miswired connections in the developing brain, and many experts believe that therapies must begin during a “critical window,” before the faulty circuits become fixed in place. But a new study online today in Science shows that at least one malfunctioning circuit can be repaired after that window closes, holding out hope that in some forms of autism, abnormal circuits in the brain can be corrected even after their development is complete.
Faulty wiring. Shutting off the Nlgn3 gene in mice (right panel) results in miswired synaptic connections, which may be fixable. Credit: S. J. Baudouin et al., Science
According to developmental neurobiologist Peter Scheiffele of the University of Basel in Switzerland, autism doesn’t result from a handful of “culprit” genes that point to a treatable flaw. Instead, patients appear to carry mutations in one out of dozens, even hundreds of risk genes. “This genetic complexity is a huge issue with respect to developing treatments [for autism],” Scheiffele says. To complicate the picture further, autism is not always an isolated disorder; it’s often a common feature in syndromes that otherwise differ drastically. For example, in fragile X syndrome, a form of mental retardation, about 25% of patients are also autistic.
Scheiffele and colleagues were studying a gene called neuroligin-3 (Nlgn3), involved in building the contact points, called synapses, between neurons. Many researchers believe that autism begins at the synapse, and mutations in Nlgn3 have appeared in some forms of the disorder. Sheiffele’s team was focusing on synapses in the cerebellum, a part of the brain that controls movement, but, according to recent research, may also be involved in social behavior. Abnormalities in this region may contribute to both the unusual movements and the social problems seen in autistic patients.
To get a better handle on the role of Nlgn3, the scientists studied mice whose Nlgn3 genes were engineered with an on-off switch, called a promoter region, that is controlled by the antibiotic doxycycline. The animals were raised with the drug in their drinking water, which kept the switch in the off position. With the Nlgn3 gene disabled in the mice, neurons in their cerebellum made the abnormal connections seen in the autistic brain.
Specifically, and much to the researchers’ surprise, the lack of Nlgn3 led to the overactivation of a receptor abbreviated as mGluR1α. This receptor is a component of a pathway that is also disrupted in fragile X syndrome, though it results from mutations in an entirely different gene. In the mice, the overabundance of these receptors led the neurons to make synaptic connections in the wrong places.
To see if turning Nlgn3 gene back on would correct these problems, the researchers withdrew the doxycycline. It worked: With Nlgn3 functioning once more, levels of the extraneous receptor receded back to normal, and the misplaced synapses began to disappear.
"Our finding demonstrates that there is still flexibility after the ‘critical window’ of brain development,” Scheiffele says. “It raises the question: To what extent can a miswired brain be corrected?” The next step, he says, is to see whether motor abnormalities, such as ladder-climbing difficulties, and social interactions can be corrected with similar treatment in the engineered mice. His team is also studying whether drugs that block the mGluR1α receptor can have the same effect as genetically controlling the Nlgn3 gene, which isn’t a treatment option for humans.
"This study holds out hope for children and even adults with developmental disorders. Maybe their conditions aren’t set in stone and can be treated," says neuroscientist Kimberly Huber of the University of Texas Southwestern Medical Center in Dallas. Huber adds that drugs that block a similar receptor, mGluR5, are in clinical trials to treat fragile X syndrome.
(Source: news.sciencemag.org)
Filed under brain autism psychology neuroscience genetics neuroligin-3 science
