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IBM Research Thinks It's Solved Why The Brain Uses So Much Energy
• popsci.comWe don't know much about the brain. Scientists and researchers have poked and prodded parts of our most complex organ for centuries, giving names to the most obvious parts. But we still lack answers to fundamental questions, like what the brain does with most of its energy, or how diseases make neurons in the brain affect each other.
A researcher at IBM has uncovered what could be a start to these answers: a model for what the brain does at rest, when it's not reading or thinking or cooking you breakfast. IBM neuroscientist James Kozloski calls it "the Grand Loop."
"The brain consumes a great amount of energy doing nothing. It's a great mystery of neuroscience," Kozloski said. "You don't spend that much energy on noise unless there's a really good reason."
1 Comments in Response to IBM Research Thinks It's Solved Why The Brain Uses So Much Energy
For anyone who might be interested in neurological disease related to this sort of thing, Internet search on "prion."
From Scientific American (http://www.scientificamerican.com/article/what-is-a-prion-specifica/):
"'Prion' is a term first used to describe the mysterious infectious agent responsible for several neurodegenerative diseases found in mammals, including Creutzfeldt-Jakob disease (CJD) in humans. The word itself derives from 'proteinaceous infectious particle'; it refers to the initially heretical hypothesis that the infectious agent causing those diseases consists only of protein, with no nucleic acid genome. (All previously known pathogens, such as bacteria and viruses, contain nucleic acids, which enable them to reproduce.) The prion hypothesis explained why the mysterious infectious agent is resistant to ultraviolet radiation, which breaks down nucleic acids, but is susceptible to substances that disrupt proteins.
"A major breakthrough occurred when researchers discovered that the infectious agent consists primarily of a protein found in the membranes of normal cells, but in this case the protein has an altered shape, or conformation. Some scientists hypothesized that the distorted protein could bind to other proteins of the same type and induce them to change their conformation as well, producing a chain reaction that propagates the disease and generates new infectious material. Since then, the gene for this protein has been successfully cloned, and studies using transgenic mice have bolstered the prion hypothesis. The evidence in support of the hypothesis is now very strong, though not incontrovertible.
"Research on prion diseases has recently accelerated for several reasons. First, the mounting experimental evidence has generated great interest in what appears to be a totally new kind of mechanism of disease. Second, the demonstration that prions are responsible for 'mad cow' disease (bovine spongiform encephalopathy), which has infected large numbers of cattle in Great Britain and panicked the public, has lent new urgency to the quest for a cure--especially since the discovery that infected cows might be responsible for several new cases of CJD in humans. ..."