Intel has invested large amounts of money on research and development of thought-controlled devices, otherwise known as brain-computer interfaces. Research is underway to determine the best way to harness the power of thought. The internal method requires a craniotomy to implant electrodes in or upon the brain, while the external method consists of applying electrodes to the scalp to monitor brainwaves.
The implications of the research could hold many benefits for spinal cord injury sufferers and traumatic brain injury survivors. Electrodes implanted directly into a patient’s brain may control prosthetic limbs of the near future. The devices might even include some kind of sensors to simulate the sensation of touch along the prosthetic skin.
Monitoring devices grow increasingly complex, as companies develop computers that can collect psychological data. Attention Control Systems Inc. is developing a bot that will, “collect psychological data, detect panic attacks and measure psychological symptoms,” according to the Wired article.
For veterans suffering with the symptoms of traumatic brain injury, the military has invested in high-tech schedulers to remind patients to complete various tasks, to help them stay focused throughout the day, and to monitor their movement and give them prompts when necessary.
With current advances in neurology, electronics, brain-computer interfaces, wireless technology, biotechnology, genetics, stem cells, and prosthetics, the future looks bright for spinal cord injury and traumatic brain injury survivors.
Atul Gawande: I’m a surgeon at the Brigham and Women’s Hospital in Boston, associate professor at the Harvard School of Public Health, and a writer for The New Yorker magazine.
A scientific group led by the Translational Genomics Research Institute (TGen) have identified three kinases, or proteins, that dismantle connections within brain cells, which may lead to memory loss associated with Alzheimer’s disease.
These findings, the results of a multi-year TGen study, are published in this month’s edition of BMC Genomics in a paper titled: High-content siRNA screening of the kinome identifies kinases involved in Alzheimer’s disease-related tau hyperphosphorylation.
The three kinases were found to cause a malfunction in tau, a protein critical to the formation of the microtubule bridges within brain cells, or neurons. These bridges support the synaptic connections that, like computer circuits, allow neurons to communicate with each other.
“The ultimate result of tau dysfunction is that neurons lose their connections to other neurons, and when neurons are no longer communicating, that has profound effects on cognition – the ability to think and reason,” said Dr. Travis Dunckley, an Associate Investigator in TGen’s Neurodegenerative Research Unit and the scientific paper’s senior author.
Tau performs a critical role in the brain by helping bind together microtubules, which are sub-cellular structures that create scaffolding in the neurons, allowing them to stretch out along bridges called axons. The axons su
pport the synaptic, or chemical, connections with other neurons.
Under normal circumstances, kinases regulate tau by adding phosphates. This process, called tau phosphorylation, enables the microtubules to unbind and then bind again, allowing brain cells to connect and reconnect with other brain cells.
“That facilitates synaptic plasticity. It facilitates the ability of people to form new memories – to form new connections between different neurons – and maintain those memories. So, it’s an essential function,” Dr. Dunckley said.
However, sometimes the tau protein becomes hyperphosphorylated, a condition in which the tau creates neurofibrillary tangles, one of the signature indicators of Alzheimer’s.
“When tau protein is hyperphosphorylated, the microtubule comes apart – basically destroying that bridge – and the neurons can no longer communicate with each other,” Dr. Dunckley said.
TGen investigators created sophisticated tests to look at all 572 known and theoretical kinases within human cells. They identified 26 associated with the phosphorylation of tau. Of these 26, three of them – EIF2AK2, DYRK1A and AKAP13 – were found to cause hyperphosphorylation of tau, permanently dismantling the microtubule bridges.
“This paper shows, for the first time, these three kinases affect Alzheimer’s disease-relevant tau hyperphosphorylation, in which most of the tau protein is now driven into a permanently phosphorylated form,” Dr. Dunckley said.
The next step will be to identify drug compounds that can negate the effects of the three kinases linked to tau hyperphosphorylation.
“The reason that we did this study was to identify therapeutic targets for Alzheimer’s disease, whereby we could modify the progression of tau pathology,” Dr. Dunckley said. “This was a screen to identify what the relevant targets are. Now, we want to match those targets to treatments.”
Despite clear and disabling difficulties in day-to-day living, Peek accumulated an encyclopaedic knowledge of numerous subjects areas, could read two pages of a book at once and could instantly calculate the day of the week for any given date.
For many years Peek was thought to have autism, but scans completed in 1988 by neuroscientist Daniel Christensen and colleagues indicated that there were significant brain abnormalities, most strikingly a malformed cerebellum and an absence of the corpus callosum – the bundle of fibres that connect the two hemispheres of the brain.
Among other findings, this suggested that the most likely diagnosis was a genetic condition called FG syndrome.
He was also the subject of numerous documentaries and you can view one of the best of them, Kim Peek – The Real Rain Man, on YouTube.
UPDATE: SciAm have made their article on Kim Peek freely available on their website as a tribute.
Link to announcement from Nature.com.
pdf of excellent SciAm article ‘Inside the mind of a savant’.
Link to documentary Kim Peek – The Real Rain Man.
A study in the Proceedings of the National Academy of Sciences finds that endocannabinoids, compounds naturally found in the body related to pot’s active ingredient, could inform the effort to control appetite.
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Question: why are so many leading modern scientists so dull and lacking in scientific ambition? Answer: because the science selection process ruthlessly weeds-out interesting and imaginative people. At each level in education, training and career progression there is a tendency to exclude smart and creative people by preferring Conscientious and Agreeable people. The progressive lengthening of scientific training and the reduced independence of career scientists have tended to deter vocational ‘revolutionary’ scientists in favour of industrious and socially adept individuals better suited to incremental ‘normal’ science. High general intelligence (IQ) is required for revolutionary science. But educational attainment depends on a combination of intelligence and the personality trait of Conscientiousness; and these attributes do not correlate closely. Therefore elite scientific institutions seeking potential revolutionary scientists need to use IQ tests as well as examination results to pick-out high IQ ‘under-achievers’. As well as high IQ, revolutionary science requires high creativity. Creativity is probably associated with moderately high levels of Eysenck’s personality trait of ‘Psychoticism’. Psychoticism combines qualities such as selfishness, independence from group norms, impulsivity and sensation-seeking; with a style of cognition that involves fluent, associative and rapid production of many ideas. But modern science selects for high Conscientiousness and high Agreeableness; therefore it enforces low Psychoticism and low creativity. Yet my counter-proposal to select elite revolutionary scientists on the basis of high IQ and moderately high Psychoticism may sound like a recipe for disaster, since resembles a formula for choosing gifted charlatans and confidence tricksters. A further vital ingredient is therefore necessary: devotion to the transcendental value of Truth. Elite revolutionary science should therefore be a place that welcomes brilliant, impulsive, inspired, antisocial oddballs – so long as they are also dedicated truth-seekers.
“We have shown in an animal model that dietary intervention can restore a proper balance of neurochemicals in the injured part of the brain, and simultaneously improves cognitive performance,” said study leader Akiva S. Cohen, Ph.D., a neuroscientist at The Children’s Hospital of Philadelphia.
If these results in mice can be translated to human medicine, there would be a broad clinical benefit. Every 23 seconds, a man, woman or child in the United States suffers a traumatic brain injury (TBI). The primary cause of death and disability in children and young adults, TBI also accounts for permanent disabilities in more than 5 million Americans. The majority of those cases are from motor vehicle injuries, along with a rising incidence of battlefield casualties.
Although physicians can relieve the dangerous swelling that occurs after a TBI, there are currently no treatments for the underlying brain damage that brings in its wake cognitive losses in memory, learning and other functions.
The animals in the current study received a cocktail of three branched chain amino acids (BCAAs), specifically leucine, isoleucine and valine, in their drinking water. Previous researchers had shown that people with severe brain injuries showed mild functional improvements after receiving BCAAs through an intravenous line.