Posts tagged brain

Posts tagged brain
Purkinje neurons (yellow) generated from embryonic stem cells integrate into the cerebellum (red) when transplanted into the fetal mouse brain.
© 2010 K. Muguruma et al.
Ray Kurzweil, the bold futurist and author of The New York Times bestseller "The Singularity Is Near", is arguably today’s most influential technological visionary. A pioneering inventor and theorist, he has explored for decades how artificial intelligence can enrich and expand human capabilities.
Now, in his much-anticipated How to Create a Mind, he takes this exploration to the next step: reverse-engineering the brain to understand precisely how it works, then applying that knowledge to create vastly intelligent machines.
Drawing on the most recent neuroscience research, his own research and inventions in artificial intelligence, and compelling thought experiments, he describes his new theory of how the neocortex (the thinking part of the brain) works: as a self-organizing hierarchical system of pattern recognizers. Kurzweil shows how these insights will enable us to greatly extend the powers of our own mind and provides a roadmap for the creation of superintelligence—humankind’s most exciting next venture. We are now at the dawn of an era of radical possibilities in which merging with our technology will enable us to effectively address the world’s grand challenges.
How to Create a Mind is certain to be one of the most widely discussed and debated science books in many years—a touchstone for any consideration of the path of human progress.
Futurist Ray Kurzweil believes that the cloud will help expand the capacity of the human brain beyond its current limitations.
Futurist and author Ray Kurzweil predicts the cloud will eventually do more than store our emails or feed us streaming movies on demand: it’s going to help expand our brain capacity beyond its current limits.
In a question-and-answer session following a speech to the DEMO technology conference in Santa Clara, California last week, Kurzweil described the human brain as impressive but limited in its capacity to hold information. “By the time we’re even 20, we’ve filled it up,” he said, adding that the only way to add information after that point is to “repurpose our neocortex to learn something new.” (Computerworld has posted up the full video of the talk.)
The solution to overcoming the brain’s limitations, he added, involves “basically expanding our brains into the cloud.”
Kurzweil is one of the more prominent advocates of the technological Singularity, or the idea that computers will become super-intelligent and self-replicating, essentially reducing human progress to a sideshow. He is an optimist in this scenario, arguing in talks and books that the Singularity will effectively make humanity immortal by allowing us to transfer our consciousness into non-organic systems.
Washington State University researchers have developed a new drug candidate that dramatically improves the cognitive function of rats with Alzheimer’s-like mental impairment.
Their compound, which is intended to repair brain damage that has already occurred, is a significant departure from current Alzheimer’s treatments, which either slow the process of cell death or inhibit cholinesterase, an enzyme believed to break down a key neurotransmitter involved in learning and memory development.
Such drugs, says Joe Harding, a professor in WSU’s College of Veterinary Medicine, are not designed to restore lost brain function, which can be done by rebuilding connections between nerve cells.
"This is about recovering function,” he says. "That’s what makes these things totally unique. They’re not designed necessarily to stop anything. They’re designed to fix what’s broken. As far as we can see, they work.”
Harding, College of Arts and Sciences Professor Jay Wright and other WSU colleagues report their findings in the online “Fast Forward” section of the Journal of Pharmacology and Experimental Therapeutics.
(Source: news.wsu.edu)
The Marshmallow Study Revisited
For the past four decades, the “marshmallow test” has served as a classic experimental measure of children’s self-control: will a preschooler eat one of the fluffy white confections now or hold out for two later?
Now a new study demonstrates that being able to delay gratification is influenced as much by the environment as by innate ability. Children who experienced reliable interactions immediately before the marshmallow task waited on average four times longer—12 versus three minutes—than youngsters in similar but unreliable situations [Video]
"Our results definitely temper the popular perception that marshmallow-like tasks are very powerful diagnostics for self-control capacity," says Celeste Kidd, a doctoral candidate in brain and cognitive sciences at the University of Rochester and lead author on the study to be published online October 11 in the journal Cognition.
Three studies conducted as part of Wayne State University’s Systems Biology of Epilepsy Project (SBEP) could result in new types of treatment for the disease and, as a bonus, for behavioral disorders as well.
The SBEP started out with funds from the President’s Research Enhancement Fund and spanned neurology, neuroscience, genetics and computational biology. It since has been supported by multiple National Institutes of Health-funded grants aimed at identifying the underlying causes of epilepsy, and it is uniquely integrated within the Comprehensive Epilepsy Program at the Wayne State School of Medicine and the Detroit Medical Center.
Under the guidance of Jeffrey Loeb, M.D., Ph.D., associate director of the Center for Molecular Medicine and Genetics (CMMG) and professor of neurology, the project brings together researchers from different fields to create an interdisciplinary research program that targets the complex disease. The multifaceted program at Wayne State is like no other in the world, officials say, with two primary goals: improving clinical care and creating novel strategies for diagnosis and treatment of patients with epilepsy.
(Source: research.wayne.edu)
Target for obesity drugs comes into focus
Researchers at the University of Michigan have determined how the hormone leptin, an important regulator of metabolism and body weight, interacts with a key receptor in the brain.
Leptin is a hormone secreted by fat tissue that has been of interest for researchers in obesity and Type 2 diabetes since it was discovered in 1995. Like insulin, leptin is part of a regulatory network that controls intake and expenditure of energy in the body, and a lack of leptin or resistance to it has been linked to obesity in people.
Although there can be several complex reasons behind leptin resistance, in some cases the underlying cause is malfunction of the leptin receptor in the brain. An understanding of how leptin and its receptor interact could lead to new treatments for obesity and metabolic disorders, but the structure of this signaling complex has evaded researchers for years.
Georgios Skiniotis, a faculty member at the Life Sciences Institute and assistant professor in biological chemistry at the U-M Medical School, employed electron microscopy to obtain the first picture of the interaction between leptin and its receptor.
Skiniotis also traced similarities between the leptin receptor and other receptors of the same family, which may provide insight into new targets for treatment of other hormone-related diseases.
Engineered flies spill secret of seizures
In a newly reported set of experiments that show the value of a particularly precise but difficult genetic engineering technique, researchers at Brown University and the University of California–Irvine have created a Drosophila fruit fly model of epilepsy to discern the mechanism by which temperature-dependent seizures happen.
The researchers used a technique called homologous recombination — a more precise and sophisticated technique than transgenic gene engineering — to give flies a disease-causing mutation that is a direct analogue of the mutation that leads to febrile epileptic seizures in humans. They observed the temperature-dependent seizures in whole flies and also observed the process in their brains. What they discovered is that the mutation leads to a breakdown in the ability of certain cells that normally inhibit brain overactivity to properly regulate their electrochemical behavior.
In addition to providing insight into the neurology of febrile seizures, said Robert Reenan, professor of biology at Brown and a co-corresponding author of the paper in the Journal of Neuroscience, the study establishes
“This is the first time anyone has introduced a human disease-causing mutation overtly into the same gene that flies possess,” Reenan said.
Scientists at the University of Bath are one step further to understanding the role of one of the proteins that causes the neurodegenerative disorder, Amyotrophic Lateral Sclerosis (ALS), also known as Motor Neurone Disease (MND).

The scientists studied a protein called angiogenin, which is present in the spinal cord and brain that protects neurones from cell death. Mutations in this protein have been found in sufferers of MND and are thought to play a key role in the progression of the condition.
MND triggers progressive weakness, muscle atrophy and muscle twitches and spasms. The disease affects around 5000 people in the UK.
The team of cell biologists and structural biologists have, for the first time, produced images of the 3D structures of 11 mutant versions of angiogenin to see how the mutations changed the structure of the active part of the molecule, damaging its function.
The study, published in the prestigious journal Nature Communications, provides insights into the causes of this disease and related conditions such as Parkinson’s Disease.
The team also looked at the effects of the malfunctioning proteins on neurones grown from embryonic stem cells in the laboratory.
They found that some of the mutations stopped the protein being transported to the cell nucleus, a process that is critical for the protein to function correctly.
The mutations also prevented the cells from producing stress granules, the neurone’s natural defence from stress caused by low oxygen levels.
Dr Vasanta Subramanian, Reader in Biology & Biochemistry at the University, said:
“This study is exciting because it’s the first time we’ve directly linked the structure of these faulty proteins with their effects in the cell.
“We’ve worked alongside Professor Ravi Acharya’s group to combine structural knowledge with cell biology to gain new insights into the causes of this devastating disease.
“We hope that the scientific community can use this new knowledge to help design new drugs that will bind selectively to the defective protein to protect the body from its damaging effects.”
The findings were welcomed by medical research charity, the Motor Neurone Disease (MND) Association, the only national charity in England, Wales and Northern Ireland dedicated to supporting people living with MND while funding and promoting cutting-edge global research to bring about a world free of the disease.
Dr Brian Dickie, Director of Research Development at the charity, said: “The researchers at the University of Bath have skilfully combined aspects of biology, chemistry and physics to answer some fundamental questions on how angiogenin can damage motor neurones. It not only advances our understanding of the disease, but may also give rise to new ideas on treatment development.”
(Source: bath.ac.uk)