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One of the #brain’s mysteries is how exactly it reorganizes new #information as you learn new tasks. The standard to date was to test how neurons learned new behavior one #neuron at a time. Carnegie Mellon University and the University of Pittsburgh decided to try a different approach. They looked at the population of neurons to see how they worked together while #learning a new behavior. Studying the intracortical population activity in the primary motor cortex of rhesus macaques during short-term learning in a brain–computer interface (BCI) task, they were able to study the reorganization of population during learning. Their new research indicates that when the brain learns a new activity that it is less flexible than previously thought. The researchers were able to draw strong hypothesis about neural reorganization during learning by using BCI. Through the use of BCI the mapping between #neural activity and learning is completely known.

“In this experimental paradigm, we’re able to track all of the neurons that can lead to behavioral improvements and look at how they all change simultaneously,” says Steve Chase, an associate professor of biomedical engineering at Carnegie Mellon and the Center for the Neural Basis of #Cognition. “When we do that, what we see is a really constrained set of changes that happen, and it leads to this suboptimal improvement of performance. And so, that implies that there are limits that constrain how flexible your brain is, at least on these short time scales.”

It is often challenging to learn new tasks quickly that require a high level of proficiency. Neural plasticity is even more constrained than previously thought as results of this research indicate.

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Imagine being able to treat neurodegenerative diseases and mental disorders such as Alzheimer’s disease, Parkinson’s, epilepsy, PTSD, depression, and anxiety with non-invasive light-based therapy. This is the quest of pioneering scientists and researchers in optogenetics, an emerging field in biotechnology that uses light to control cells in living tissues such as neurons, in order to study brain function.

British Nobel laureate Francis Crick of The Salk Institute for Biological Studies in La Jolla, California put forth the concept of the ability to turn the firing of “one or more types of neuron on and off in the alert animal in a rapid manner” by using light as “the ideal signal” in his paper “The impact of molecular biology on neuroscience” published in Philosophical Transactions of the Royal Society B in 1999. Crick noted that his concept might be somewhat “far-fetched.” Yet as improbable as it would seem to the brightest minds in science before the turn of the century, this idea was proven in a little over half a decade.

In optogenetics, scientists add genetic code to target tissue, typically a neuron, which enables it to make light-responsive proteins called opsins. Gero Miesenböck and Boris Zemelman published a study in 2002 titled “Selective photostimulation of genetically charged neurons” in Neuron. They used opsin from the retina of a fruit fly to make a neuron light-sensitive. A year later, they demonstrated the use of heterologous proteins to sensitize neurons to light [1]. Peter Hegemann, Georg Nagel and other researchers published their discovery of phototaxis and photophobic responses of green algae in 2002 [2]. In August 2005, MIT neuroscientist Ed. Boyden, PhD, along with Karl Deisseroth, Feng Zhang, Georg Nagel, and Ernst Bamberg published in Nature Neuroscience a landmark breakthrough in optogenetics, “Millisecond-timescale, genetically targeted optical control of neural activity.

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The second part of LEAF’s interview with the SENS Research Foundation team is out!


Welcome to part two of our three-part Undoing Aging 2018 interview of Dr. Aubrey de Grey and his team at SENS Research Foundation. Today, we have some of the scientific questions that the community had about SENS; there are some very detailed responses, and we hope you enjoy them.

Regarding the use of senolytics, are you concerned about their potential to remove highly specialized cells like cardiomyocytes, which do not divide or do so very slowly? Could taking senolytics without the ability to replace these specialized lost cells be risky unless combined with replacement therapies?

Aubrey: This is not a major concern, for a few reasons. First, when cells turn senescent, they cease carrying out their specialized function (as a cardiomyocyte, or neuron, or what have you), so no such function is lost by ablating them. Second, cells that don’t divide (like cardiomyocytes and neurons) are far less likely to become senescent in the first place than cell types that divide; many of the main drivers of senescence are related to cell division. And third, in the specific case of cardiomyocytes, there’s already significant evidence in rodents that it improves cardiac function overall [1] as well as wider cardiovascular health [2–3].

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A SILICON Valley billionaire is paying the ultimate price for the chance of immortality: death.

Well that, and a spare ten grand.

Entrepreneur Sam Altman is one of 25 people who have splashed the cash to join a waiting list at Nectome – a startup that promises to upload your brain into a computer to grant eternal life to your consciousness.

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I ntelligence could be measured with a swab of saliva, or drop of blood, after scientists showed for the first time that a person’s IQ can be predicted just by studying their DNA.

In the largest ever study looking at the genetic basis for intelligence, researchers at the University of Edinburgh and Harvard University discovered hundreds of new genes linked to brain power.

Previous studies have suggested that between 50 per cent and 75 per cent of intelligence is inherited, and the rest comes through upbringing, friendship groups and education. That figure was calculated by studying identical twins who share the same DNA, therefore any differences in IQ between them must be non-genetic.

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