American Indians who use the hallucinogen peyote regularly in connection with religious ceremonies show no evidence of brain damage or psychological problems, report researchers at Harvard-affiliated McLean Hospital.
Jülich, 10 October 2013 – The human brain keeps changing throughout a person’s lifetime. New connections are continually created while synapses that are no longer in use degenerate.
To date, little is known about the mechanisms behind these processes. Jülich neuroinformatician Dr. Markus Butz has now been able to ascribe the formation of new neural networks in the visual cortex to a simple homeostatic rule that is also the basis of many other self-regulating processes in nature. With this explanation, he and his colleague Dr. Arjen van Ooyen from Amsterdam also provide a new theory on the plasticity of the brain – and a novel approach to understanding learning processes and treating brain injuries and diseases.
The brains of adult humans are by no means hard wired. Scientists have repeatedly established this fact over the last few years using different imaging techniques. This so-called neuroplasticity not only plays a key role in learning processes, it also enables the brain to recover from injuries and compensate for the loss of functions. Researchers only recently found out that even in the adult brain, not only do existing synapses adapt to new circumstances, but new connections are constantly formed and reorganized. However, it was not yet known how these natural rearrangement processes are controlled in the brain. In the open-access journal PLOS Computational Biology, Butz and van Ooyen now present a simple rule that explains how these new networks of neurons are formed.
"It’s very likely that the structural plasticity of the brain is the basis for long-term memory formation," says Markus Butz, who has been working at the recently established Simulation Laboratory Neuroscience at the Jülich Supercomputing Centre for the past few months. "And it’s not just about learning. Following the amputation of extremities, brain injury, the onset of neurodegenerative diseases, and strokes, huge numbers of new synapses are formed in order to adapt the brain to the lasting changes in the patterns of incoming stimuli."
These results show that the formation of new synapses is driven by the tendency of neurons to maintain a 'pre-set' electrical activity level. If the average electric activity falls below a certain threshold, the neurons begin to actively build new contact points. These are the basis for new synapses that deliver additional input – the neuron firing rate increases. This also works the other way round: as soon as the activity level exceeds an upper limit, the number of synaptic connections is reduced to prevent any overexcitation – the neuron firing rate falls. Similar forms of homeostasis frequently occur in nature, for example in the regulation of body temperature and blood sugar levels.
"It was previously assumed that structural plasticity also follows the principle of Hebbian plasticity. The findings suggest that structural plasticity is governed by the homeostatic principle instead, which was not taken into consideration before," says Prof. Abigail Morrison, head of the Simulation Laboratory Neuroscience at Jülich. Her team is already integrating the new rule into the freely accessible simulation software NEST, which is used by numerous scientists worldwide.
These findings are also of relevance for the Human Brain Project. Neuroscientists, medical scientists, computer scientists, physicists, and mathematicians in Europe are working hand in hand to simulate the entire human brain on high-performance computers of the next generation in order to better understand how it functions. “Due to the complex synaptic circuitry in the human brain, it’s not plausible that its fault tolerance and flexibility are achieved based on static connection rules. Models are therefore required for a self-organization process,” says Prof. Markus Diesmann from Jülich’s Institute of Neuroscience and Medicine, who is involved in the project. He heads Computational and Systems Neuroscience (INM-6), a subinstitute working at the interface between neuroscientific research and simulation technology.
The brain, with its billions of interconnected neurons, is without any doubt the most complex organ in the body and it will be a long time before we understand all its mysteries. The Human Brain Project proposes a completely new approach. The project is integrating everything we know about the brain into computer models and using these models to simulate the actual working of the brain. Ultimately, it will attempt to simulate the complete human brain. The models built by the project will cover all the different levels of brain organisation -- from individual neurons through to the complete cortex. The goal is to bring about a revolution in neuroscience and medicine and to derive new information technologies directly from the architecture of the brain.
The challenges facing the project are huge. Neuroscience alone produces more than 60'000 scientific papers every year. From this enormous mass of information, the project will have to select and harmonise the data it is going to use -- ensuring that data produced with different methods is fully comparable.
The data feeding the project's simulation effort will come from the clinic and from neuroscience experiments. As we try to fit all the information together, we will discover many of the brain's fundamental design secrets: the geometry and electrical behaviour of different classes of neurons, the way they connect to form circuits, and the way new functions emerge as more and more neurons connect. It is these principles, translated into mathematics that will drive the project's models and simulations.
Today, simulating a single neuron requires the full power of a laptop computer. But the brain has billions of neurons and simulating all them simultaneously is a huge challenge. To get round this problem, the project will develop novel techniques of multi-level simulation in which only groups of neurons that are highly active are simulated in detail. But even in this way, simulating the complete human brain will require a computer a thousand times more powerful than the most powerful machine available today. This means that some of the key players in the Human Brain Project will be specialists in supercomputing. Their task: to work with industry to provide the project with the computing power it will need at each stage of its work.
The Human Brain Project will impact many different areas of society. Brain simulation will provide new insights into the basic causes of neurological diseases such as autism, depression, Parkinson's, and Alzheimer's. It will give us new ways of testing drugs and understanding the way they work. It will provide a test platform for new drugs that directly target the causes of disease and that have fewer side effects than current treatments. It will allow us to design prosthetic devices to help people with disabilities. The benefits are potentially huge. As world populations grow older, more than a third will be affected by some kind of brain disease. Brain simulation provides us with a powerful new strategy to tackle the problem.
The project also promises to become a source of new Information Technologies. Unlike the computers of today, the brain has the ability to repair itself, to take decisions, to learn, and to think creatively - all while consuming no more energy than an electric light bulb. The Human Brain Project will bring these capabilities to a new generation of neuromorphic computing devices, with circuitry directly derived from the circuitry of the brain. The new devices will help us to build a new generation of genuinely intelligent robots to help us at work and in our daily lives.
The Human Brain Project builds on the work of the Blue Brain Project. Led by Henry Markram of the Ecole Polytechnique Fédérale de Lausanne (EPFL), the Blue Brain Project has already taken an essential first towards simulation of the complete brain. Over the last six years, the project has developed a prototype facility with the tools, know-how and supercomputing technology necessary to build brain models, potentially of any species at any stage in its development. As a proof of concept, the project has successfully built the first ever, detailed model of the neocortical column, one of the brain's basic building blocks.
Human Brain Project The multi-billion Euro Human Brain Project, co-funded by the European Union, plans to use supercomputers to model the human brain and then use the research to simulate... [[ This is a content summary only.
What's in a face? Researchers find patterns of neural activity in brain region ... Medical Xpress Using real-time scans of the brain, recent Harvard Ph.D. Juan Manuel Contreras, Richard Clarke Cabot Professor of Social Ethics Mahzarin R.
By hijacking connections between neurons deep within the brain, scientists forced full mice to keep eating and hungry mice to shun food. By identifying precise groups of cells that cause eating and others that curb it, the results begin to clarify the intricate web of checks and balances in the brain that control feeding.
“This is a really important missing piece of the puzzle,” says neuroscientist Seth Blackshaw of Johns Hopkins University in Baltimore. “These are cell types that weren’t even predicted to exist.” A deeper understanding of how the brain orchestrates eating behavior could lead to better treatments for disorders such as anorexia and obesity, he says.
Scientists led by Joshua Jennings and Garret Stuber of the University of North Carolina at Chapel Hill genetically tweaked mice so that a small group of neurons would respond to light. When a laser shone into the brain, these cells would either fire or, in a different experiment, stay quiet. These neurons reside in a brain locale called the bed nucleus of the stria terminalis, or BNST. Some of the message-sending arms of these neurons reach into the lateral hypothalamus, a brain region known to play a big role in feeding.
When a laser activated these BNST neurons, the mice became ravenous, voraciously eating their food, the researchers report in the Sept. 27, 2013 Science. “As soon as you turn it on, they start eating and they don’t stop until you turn it off,” Stuber says. The opposite behavior happened when a laser silenced BNST neurons’ messages to the lateral hypothalamus: The mice would not eat, even when hungry.
The results illuminate a complex network of neuron connections, in which some cells boost other neurons’ activity, while other cells apply brakes. In the experiment, stimulating BNST neurons with light — which consequently shut down the activity of neurons in the lateral hypothalamus — led to the overeating behavior, the team found. That result suggests that these lateral hypothalamus neurons normally restrict feeding.
That finding is surprising, says Blackshaw. Earlier experiments hinted that these hypothalamic cells would encourage eating behavior, but the new study suggests the exact opposite.
The researchers don’t know whether, if they controlled the neurons for long periods, the mice would ultimately starve or overeat to the point of illness. Stuber and colleagues used the laser technique, called optogenetics, in roughly 20-minute bursts. Longer-term manipulations of these neural connections — perhaps using a drug — might cause lasting changes in appetite and, as a result, body mass, Stuber says.
This precise control of feeding behavior underscores the fact that eating disorders occur when brain systems go awry, Stuber says. “We think of feeding in terms of metabolism and body stuff,” he says. “But at the end of the day, it’s controlled by the brain.”
APOE Plasma Levels Predict Dementia Independent of Genotype
Daniel M. Keller, PhD
Oct 04, 2013
VIENNA, Austria — Association of the apolipoprotein E ε4 (APOE) allele and greatly elevated risk of developing Alzheimer's disease emerged 2 decades ago. But a recent study indicates that the level of APOE in plasma, independent of genotype, is also a marker of risk, in this case, greater risk with lower levels.
"There was no evidence of interaction between APOE level and APOE genotype in predicting Alzheimer's disease," Katrine Rasmussen, MD, from the Department of Clinical Biochemistry at the Rigshospitalet of the University of Copenhagen, Denmark, reported. "It was the same in each [APOE] genotype."
APOE, a product of astrocytes, has a major role in lipid transport and in neuronal repair. It carries cholesterol to APOE low-density lipoprotein receptors on neurons.
Speaking here at the XXI World Congress of Neurology (WCN), Dr. Rasmussen presented a study of 75,708 participants in the Copenhagen General Population Study and the Copenhagen City Heart Study to test the association of plasma APOE levels and APOE genotype with the development of dementia.
The researchers measured APOE levels and genotyped the samples for the rs429358 and rs7412 genes. These genes combine to produce 6 common APOE genotypes: ε22, ε32, ε42, ε33, ε43, ε44.
When the nearly 76,000 participants were divided into APOE tertiles, the cumulative incidence of Alzheimer's disease with age was significantly associated with APOE level.
"We found a 3-fold increased risk for the lowest tertile versus the highest tertile and a highly significant [value] for trend, and the association remained after further adjustment for the APOE genotype," Dr. Rasmussen reported (log-rank trend P< .001).
APOE levels correlated with genotype (P < .001), but when multifactorial adjustment that included genotype was done, APOE level was found to be an independent risk predictor of Alzheimer's disease.
Compared with the highest tertile of APOE plasma level, the hazard ratio (HR) for the middle tertile was approximately 1.3 and for the lowest tertile approximately 1.6 (P for trend = .006).
As expected, the researchers found an association between APOE genotype and Alzheimer's disease, with the lowest risk seen with the ε22, ε 32, ε 42, and ε 33 genotypes (HR, approximately 1 after multifactorial adjustment including for APOE level; P for trend < .001).
The highest risks were seen with the ε43 and ε44 genotypes after the same adjustments (HR, approximately 3 and 7, respectively; P for trend < .001).
Even when low-risk genotypes (ε32 and ε33) were stratified by APOE level, the level was an independent risk factor for Alzheimer's disease (HR, approximately 1.9 for the lowest vs highest APOE tertile; P for trend = .001).
"We found that low plasma levels of APOE associate with risk of dementia, and we found that low plasma levels of APOE associate with risk of dementia independent of APOE gene type," Dr. Rasmussen concluded.
Session chair Jagjit Chopra, MD, PhD, professor emeritus of the Postgraduate Institute of Medical Education and Research in Chandigarh, India, who was not involved in the study, praised the study for its size and selection of populations to examine.
"This study was very good — 76,000 [participants]," he commented to Medscape Medical News. "This is not a small number of people that they looked into, and they were normal people, a normal population. That's the good part of it. They didn't say that we pick up only very elderly people."
Dr. Chopra suggested that there is a role for pharmaceutical companies to pursue the APOE finding as a possible contributor to a mechanism underlying Alzheimer's disease and a possible point of intervention leading to drug development.
There was no commercial funding for the study. Dr. Rasmussen and Dr. Chopra have disclosed no relevant financial relationships.
WCN 2013: XXI World Congress of Neurology: Free Papers Session 21. Presented September 24, 2013.
The connection between poor sleep, memory loss and brain deterioration as we grow older has been elusive. But for the first time, UC Berkeley scientists have found a link between these hallmark maladies of old age.
Sharing your scoops to your social media accounts is a must to distribute your curated content. Not only will it drive traffic and leads through your content, but it will help show your expertise with your followers.
How to integrate my topics' content to my website?
Integrating your curated content to your website or blog will allow you to increase your website visitors’ engagement, boost SEO and acquire new visitors. By redirecting your social media traffic to your website, Scoop.it will also help you generate more qualified traffic and leads from your curation work.
Distributing your curated content through a newsletter is a great way to nurture and engage your email subscribers will developing your traffic and visibility.
Creating engaging newsletters with your curated content is really easy.