Posts tagged brain
Articles and news from the latest research reports.
Study sheds light on underlying causes of impaired brain function in muscular dystrophy
8-Aug-2012
The molecular missteps that disrupt brain function in the most common form of adult-onset muscular dystrophy have been revealed in a new study published by Cell Press. Myotonic dystrophy is marked by progressive muscle wasting and weakness, as well as excessive daytime sleepiness, memory problems, and mental retardation. A new mouse model reported in the August 9 issue of the journal Neuron reproduces key cognitive and behavioral symptoms of this disease and could be used to develop drug treatments, which are currently lacking.
The red dots are the toxic RNAs accumulating in the nucleus (blue) of a myotonic dystrophy cell (these are induced pluripotent stem, or iPS, cells) and the green is a neuronal marker. Credit: Charizanis et al., Neuron.
"The new animal model reproduces important aspects of myotonic dystrophy brain disease, so this model may be useful to develop biomarkers and test future drug therapies," says senior study author Maurice Swanson of the University of Florida.
Previous studies had shown that mutated genes underlying the disease produce toxic ribonucleic acids (RNAs) during transcription, and these RNAs cause the production of incorrect forms of proteins in muscle tissue by blocking the actions of a protein called MBNL1. As a result, proteins typically found in fetal muscles increase in abundance, while the normal suite of proteins found in adult muscles decrease in number. However, until now, it was not clear whether molecular abnormalities similar to those in muscle tissue of individuals with mytonic dystrophy also occur in the brain, resulting in the cognitive neurological problems.
In the new study, Swanson and his team focused on a related protein called MBNL2, which is found in the brain. They developed a new mouse model that lacked a functional Mbnl2 gene. These animals experienced an increase in the amount of rapid eye movement sleep as well as learning and memory deficits, similar to human patients.
The researchers also found extensive evidence of toxic RNAs in the hippocampus, as well as signs that fetal proteins were being produced in the brains of adult mutants. This pattern was also evident in the autopsied brain tissue of humans who had myotonic dystrophy. “This study should accelerate our understanding of how myotonic dystrophy mutations impact brain development and function,” Swanson says.
Source: EurekAlert!
A fine-tuned combination of two existing pharmaceutical drugs has shown promise as a potential new therapy for people addicted to cocaine—a therapy that would reduce their craving for the drug and blunt their symptoms of withdrawal.
In laboratory experiments at The Scripps Research Institute, the potential therapy, which combines low doses of the drug naltrexone with the drug buprenorphine, made laboratory rats less likely to take cocaine compulsively—a standard preclinical test that generally comes before human trials.
While the two-drug combination would have to prove safe and effective for people in clinical trials before approval by the U.S. Food and Drug Administration (FDA), the work represents a significant advance in the field because there are currently no FDA-approved medications for treating cocaine addiction.
The mechanism of action of cocaine
Cocaine modifies the action of dopamine in the brain. The dopamine rich areas of the brain are the ventral tegmental area, the nucleus accumbens and the caudate nucleus – these areas are collectively known as the brain’s ‘reward pathway’. Cocaine binds to dopamine re-uptake transporters on the pre-synaptic membranes of dopaminergic neurones. This binding inhibits the removal of dopamine from the synaptic cleft and its subsequent degradation by monoamine oxidase in the nerve terminal. Dopamine remains in the synaptic cleft and is free to bind to its receptors on the post synaptic membrane, producing further nerve impulses. This increased activation of the dopaminergic reward pathway leads to the feelings of euphoria and the ‘high’ associated with cocaine use.
New Model Synapse Could Shed Light on Disorders Such as Epilepsy and Anxiety
A new way to study the role of a critical neurotransmitter in disorders such as epilepsy, anxiety, insomnia, depression, schizophrenia, and alcohol addiction has been developed by a group of scientists led by Gong Chen, an associate professor of biology at Penn State University.
The new method involves molecularly engineering a model synapse — a structure through which a nerve cell send signals to another cell. This model synapse can precisely control a variety of receptors for the neurotransmitter called GABA, which is important in brain chemistry. The research, which will be published in the Journal of Biological Chemistry on 10 August 2012, opens the door to the possibility of creating safer and more-efficient drugs that target GABA receptors and that cause fewer side effects.
The brains of people with schizophrenia may attempt to heal from the disease
7 August 2012
New NeuRA research shows that the brains of people with schizophrenia may attempt to repair damage caused by the disease, in another example of the adult brain’s capacity to change and grow.
Prof Cyndi Shannon Weickert, Dr Dipesh Joshi and colleagues from Neuroscience Research Australia studied the brains of people with schizophrenia and focussed on one of the hardest-hit regions, the orbitofrontal cortex, which is the part of the brain involved in regulating emotional and social behaviour.
Most neurons – brain cells that transmit information – are found in tissue near the surface of the brain. However, in the brains of people with schizophrenia, the team found a high density of neurons in deeper areas.
“For over a decade we’ve known about the high density of neurons in deeper brain tissue in people with schizophrenia. Researchers thought these neurons were simply forgotten by the brain, and somehow didn’t die off like they do during development in healthy people,” says Prof Shannon Weickert.
“What we now have is evidence that suggests these neurons are derived from the part of the brain that produces new neurons, and that they may be in the process of moving. We can’t be sure where they are moving to, but given their location it is likely they are on their way to the surface of the brain, the area most affected by schizophrenia,” Prof Shannon Weickert concluded.
How was this study done?
- Brain tissue from the orbitofrontal cortex from 38 people with schizophrenia and 38 people without the disease were used in this study.
- The density of interstitial neurons in the white matter, and the density of GABAergic neurons in the grey matter were measured.
- An increased density of interstitial white matter neurons in the white matter, and decreased density of GABAergic neurons in the grey matter was found.
- This pattern suggests that the migration of interstitial white matter neurons towards an area where they are lacking, because of schizophrenia, is a response to the disease.
In the journal Experimental Neurology, the scientists report the beneficial effects of so-called astrocytes, a certain type of glial cells. They get their name from the Greek word for glue, as it was long thought that these cells simply hold the nerve cells together and provided them with nutrients. In the case of epilepsy, the prevalent opinion was that their reaction to a seizure would actually damage the brain. The researchers from Freiburg disagree. In fact, they say, astrocytes help to reduce long-term damage brought upon by epileptic fits.
The team discovered the positive effects of astrocytes in mice, in which epileptic states can be selectively triggered. If the scientists injected mice with a specific protein to activate the astrocytes prior to an epilepsy-inducing insult, fewer nerve cells died in the wake of the seizure. Other pathological changes that would usually occur in the brain were likewise significantly reduced. The astrocytes’ protective effect lasted for many days after their activation. When the researchers measured the rodents’ brain activity, they likewise found fewer signs that are typical for a brain suffering from epilepsy. However, the authors report that the astrocytes had to be already activated before seizures were elicited. Activating them afterwards, on the other hand, did not lead to a protective effect.
Further studies will have to demonstrate that astrocytes have this protective influence all over the brain. According to Haas, who is also a member of Freiburg’s new cluster of excellence BrainLinks-BrainTools, their findings suggest that a timely activation of astrocytes could offer an effective protection from long-term damage to the brain.
Having an operation?
Don’t be surprised if the surgeon performs it from the room next door.
Indeed, he could even operate from halfway across the world — because these doctors are increasingly using robots to treat disease and injury.
‘These are incredibly exciting times,’ says Brian Davies, emeritus professor of medical robotics at Imperial College London and inventor of the surgical robot, which in April 1991 became the first in the world to remove tissue from a living human.
‘Robots can work much more accurately than human hands, which is fantastic now that we are seeking minimally invasive surgery through a tiny incision where precision is key,’ says Professor Davies.
Of course, the surgeon still performs the operation, but uses the robot to see inside the body, or operates it using a joystick or console so it’s like a spare arm — but without the human hand’s natural shake.
‘Medical robots are not like the sci-fi images of autonomous humanoids; they are sophisticated computer-assisted instruments that remain always under the surgeon’s control,’ says Dr Patrick Finlay, founder of medical robotics firm MediMaton.
Social Network Size Linked to Brain Size
As humans, we aren’t born with formidable armaments or defenses, nor are we the strongest, fastest, or biggest species, yet despite this we are amazingly successful. For a long time it was thought that this success was because our enlarged brains allows each of us to be smarter than our competitors: better at abstract thinking, better with tools and better at adapting our behavior to those of our prey and predators. But are these really the most significant skills our brains provide us with?
Another possibility is that we are successful because we can form long-lasting relationships with many others in diverse and flexible ways, and that this, combined with our native intelligence, explains why homo sapiens came to dominate the planet. In every way from teaching our young to the industrial division of labour we are a massively co-operative species that relies on larger and more diverse networks of relationships than any other species.
![How digital culture is rewiring our brains
Our brains are superlatively evolved to adapt to our environment: a process known as neuroplasticity. The connections between our brain cells will be shaped, strengthened and refined by our individual experiences. It is this personalisation of the physical brain, driven by unique interactions with the external world, that arguably constitutes the biological basis of each mind, so what will happen to that mind if the external world changes in unprecedented ways, for example, with an all-pervasive digital technology?
A recent survey in the US showed that more than half of teenagers aged 13 to 17 spend more than 30 hours a week, outside school, using computers and other web-connected devices. If their environment is being transformed for so much of the time into a fast-paced and highly interactive two-dimensional space, the brain will adapt, for good or ill. Professor Michael Merzenich, of the University of California, San Francisco, gives a typical neuroscientific perspective.
”There is a massive and unprecedented difference in how [digital natives’] brains are plastically engaged in life compared with those of average individuals from earlier generations and there is little question that the operational characteristics of the average modern brain substantially differ,” he says.](http://41.media.tumblr.com/tumblr_m8ft5jgs2V1rog5d1o1_400.jpg)
How digital culture is rewiring our brains
Our brains are superlatively evolved to adapt to our environment: a process known as neuroplasticity. The connections between our brain cells will be shaped, strengthened and refined by our individual experiences. It is this personalisation of the physical brain, driven by unique interactions with the external world, that arguably constitutes the biological basis of each mind, so what will happen to that mind if the external world changes in unprecedented ways, for example, with an all-pervasive digital technology?
A recent survey in the US showed that more than half of teenagers aged 13 to 17 spend more than 30 hours a week, outside school, using computers and other web-connected devices. If their environment is being transformed for so much of the time into a fast-paced and highly interactive two-dimensional space, the brain will adapt, for good or ill. Professor Michael Merzenich, of the University of California, San Francisco, gives a typical neuroscientific perspective.
”There is a massive and unprecedented difference in how [digital natives’] brains are plastically engaged in life compared with those of average individuals from earlier generations and there is little question that the operational characteristics of the average modern brain substantially differ,” he says.
Cannabis-based medications have been proved to relieve pain. This is the conclusion drawn by Franjo Grotenhermen and Kirsten Müller-Vahl in issue 29–30 of Deutsches Ärzteblatt International.
Cannabis medications can be used in patients whose symptoms are not adequately alleviated by conventional treatment. The indications are muscle spasms, nausea and vomiting as a result of chemotherapy, loss of appetite in HIV/Aids, and neuropathic pain.
The clinical effect of the various cannabis-based medications rests primarily on activation of endogenous cannabinoid receptors. Consumption of therapeutic amounts by adults does not lead to irreversible cognitive impairment. The risk is much greater, however, in children and adolescents (particularly before puberty), even at therapeutic doses.
Over 100 controlled trials of the effects of cannabinoids in various indications have been carried out since 1975. The positive results have led to official licensing of cannabis-based medications in many countries. In Germany, a cannabis extract was approved in 2011 for treatment of spasticity in multiple sclerosis. In June 2012 the Federal Joint Committee (the highest decision-making body for the joint self-government of physicians, dentists, hospitals and health insurance funds in Germany) pronounced that the cannabis extract showed a slight additional benefit for this indication and granted a temporary license until 2015.