The article is providing an answer to the following questions that are relevant to the study of intelligence:
What is “understanding”?
How can we tell whether a system has it or not? https://bit.ly/3fynqYu
#AI #MechineLearning #neuroscience #consciousness #philosophy #technology #cognition #intelligence
Xiang-Dong Fu, PhD, has never been more excited about something in his entire career. He has long studied the basic biology of RNA, a genetic cousin of DNA, and the proteins that bind it. But a single discovery has launched Fu into a completely new field: neuroscience.
For decades, Fu and his team at University of California San Diego School of Medicine studied a protein called PTB, which is well known for binding RNA and influencing which genes are turned “on” or “off” in a cell. To study the role of a protein like PTB, scientists often manipulate cells to reduce the amount of that protein, and then watch to see what happens.
But then he noticed something odd after a couple of weeks — there were very few fibroblasts left. Almost the whole dish was instead filled with neurons.
In this serendipitous way, the team discovered that inhibiting or deleting just a single gene, the gene that encodes PTB, transforms several types of mouse cells directly into neurons.
More recently, Fu and Hao Qian, PhD, another postdoctoral researcher in his lab, took the finding a big step forward, applying it in what could one day be a new therapeutic approach for Parkinson’s disease and other neurodegenerative diseases. Just a single treatment to inhibit PTB in mice converted native astrocytes, star-shaped support cells of the brain, into neurons that produce the neurotransmitter dopamine. As a result, the mice’s Parkinson’s disease symptoms disappeared.
A trove of DNA sequences from 141,456 people — and counting — offers researchers an unparalleled look at genetic variation across the general population1,2. The resource has been helping researchers to identify variants that contribute to autism since it was released online about four years ago3,4.
The genomes of autistic people harbor hundreds of potentially harmful mutations. But to firmly connect a specific variant to the condition, researchers need to see if it is common among typical people — a sign that that variant may actually be benign.
In 2014, researchers debuted one of the first tools to probe the prevalence of a mutation in the general population. Known as the Exome Aggregation Consortium (ExAC), it contained 60,000 sequences of exomes — the protein-coding regions of the genome5.
Complex behavioral phenotyping techniques are becoming more prevalent in the field of behavioral neuroscience, and thus methods for manipulating neuronal activity must be adapted to fit into such paradigms. Here, we present a head-mounted, magnetically activated device for wireless optogenetic manipulation that is compact, simple to construct, and suitable for use in group-living mice in an enriched semi-natural arena over several days. Using this device, we demonstrate that repeated activation of oxytocin neurons in male mice can have different effects on pro-social and agonistic behaviors, depending on the social context. Our findings support the social salience hypothesis of oxytocin and emphasize the importance of the environment in the study of social neuromodulators. Our wireless optogenetic device can be easily adapted for use in a variety of behavioral paradigms, which are normally hindered by tethered light delivery or a limited environment.
How does the neural activity evoked by visual stimuli support visual awareness? In this paper we report on an individual with a rare type of neural degeneration as a window into the neural responses underlying visual awareness. When presented with stimuli containing faces and target words—regardless of whether the patient was aware of their presence—the neurophysiological responses were indistinguishable. These data support the possibility that extensive visual processing, up to and including activation of identity, can occur without resulting in visual awareness of the stimuli.
Visual awareness is thought to result from integration of low- and high-level processing; instances of integration failure provide a crucial window into the cognitive and neural bases of awareness. We present neurophysiological evidence of complex cognitive processing in the absence of awareness, raising questions about the conditions necessary for visual awareness. We describe an individual with a neurodegenerative disease who exhibits impaired visual awareness for the digits 2 to 9, and stimuli presented in close proximity to these digits, due to perceptual distortion. We identified robust event-related potential responses indicating 1) face detection with the component and 2) task-dependent target-word detection with the P3b component, despite no awareness of the presence of faces or target words.
The world’s largest genetic study into chronic fatigue syndrome is to be launched in the UK after receiving £3.2m of funding from the Medical Research Council and National Institute for Health Research.
The research aims to shine a light on the debilitating long-term condition, about which little is known, by collecting DNA samples from 20,000 people who have CFS, also known as myalgic encephalomyelitis (ME).
CFS is believed to affect about 250,000 people in the UK and has been estimated to cost the economy billions of pounds each year. Individuals experience exhaustion that is not helped by rest, with one in four so severely affected they are unable to leave the house and, frequently, unable to leave their bed. Other symptoms include, pain, mental fogginess, light and noise sensitivities, as well as trouble with memory and sleep. No effective treatment exists.
New research untangles the complex code the brain uses to distinguish between a vast array of smells, offering a scientific explanation for how it separates baby powder from bleach, lemon from orange, or freshly cut grass from freshly brewed coffee.
A single scent can trigger a complex chain of events in what’s known as the olfactory bulb, the brain’s control center for smell. To unravel the intricacies of that process, researchers in the U.S. and Italy turned to a technique known as optogenetics, which uses light to control neurons in the brain. In research on mice, they used light to trick the brain into thinking it smelled a particular scent, then studied brain activity to understand the role different neurons play in a mouse’s ability to recognize that scent. Their findings were published Thursday in Science.
When we encounter a certain smell, it stimulates a specific pattern of activity among tiny spheres known as glomeruli, which are found in the olfactory bulb. The odor plays across these glomeruli like a melody across piano keys: Just as a tune is made distinct by which keys are pressed and at what point in the melody, a scent is made distinct by which glomeruli are activated and in what order.
“Despite their abundance, astrocytes have been relatively overlooked by neuroscientists,” says Mirko Santello, last author of the study. Yet these cells are extremely important to clear transmitters released by neurons. In their study the researchers were able to show that in familial migraine the astrocytes cannot remove excessive transmitters released by neurons. “The impairment in astrocytic glutamate uptake in the cingulate cortex strongly enhances cortical dendritic excitability and thus enhances firing of the neurons,” Santello says…
Migraine is a complicated disorder that affects part of the nervous system. “Our results provide a clear example of how astrocyte dysfunction produced by a genetic defect affects neuronal activity and sensitivity to head pain triggers,” explains Mirko Santello. The findings help to better understand migraine pathophysiology and suggest that the cingulate cortex may represent a critical hub in the disease. The demonstration of the link between dysfunction of astrocytes in the cingulate cortex and familial migraine could help in devising new migraine treatment strategies.
Neuroscientists of the University of Zurich shed a new light on the mechanisms responsible for familial migraine: They show that a genetic dysfunction in specific brain cells of the cingulate cortex area strongly influences head pain occurrence.
In “2030: Beyond the Film” Director Johnny Boston discusses the futurist FM-2030, the Coronavirus Pandemic, and a range of urgent issues in the medical, philosophical, longevity & futurist space with leading voices.
In this episode, Boston talks with David A. Kekich on why Kekich believes working towards Biological Superlongevity should be the first goal of Transhumanists and futurists.
About David A. Kekich: (from Maximum Life Foundation)
David Kekich is President/CEO of Maximum Life Foundation that focuses on aging research. In 1999, he realized the inevitability that science will someday control the human aging process. He understood human beings will someday be able to enjoy very long health spans by studying aging research, the root cause of most deadly diseases. The problem? He was in a race against the clock. He was faced with the possibility of being part of the “last generation to suffer from heart disease, cancer, Alzheimer’s and other aging related diseases”. His solution was to further that aging research and hopefully move it forward by establishing the Maximum Life Foundation.
Maximum Life Foundation Website:
https://www.maxlife.org/
About 2030 the film:
Johnny Boston was 10 years old when he first met FM-2030, a futurist who intended to live forever. But in 2000, after his body ceased to function, FM was cryonically preserved. 16 years later, an unexpected call places FM’s future in Johnny’s hands.
Directed By: Johnny Boston
The role genetics and gut bacteria play in human health has long been a fruitful source of scientific enquiry, but new research marks a significant step forward in unraveling this complex relationship. Its findings could transform our understanding and treatment of all manner of common diseases, including obesity, irritable bowel syndrome, and Alzheimer’s disease.
The international study, led by the University of Bristol and published today in Nature Microbiology, found specific changes in DNA — the chains of molecules comprising our genetic make-up — affected both the existence and amount of particular bacteria in the gut.
Lead author Dr David Hughes, Senior Research Associate in Applied Genetic Epidemiology, said: “Our findings represent a significant breakthrough in understanding how genetic variation affects gut bacteria. Moreover, it marks major progress in our ability to know whether changes in our gut bacteria actually cause, or are a consequence of, human disease.”