Category Archives: Neuroscience

Neuroscience

Testing the Fluorescent Proteins That Light Up the Brain – UConn Today

Neurons are cells in your brain. Shaped like little stars, they flicker and fire off signals to each other. The signals travel up and down the long tendrils, called dendrites, extending out from each point of a neurons star-shaped body. Chained into circuits like Christmas lights, neurons electrical firing forms the glimmers of our thoughts and actions.

But the process by which an individual neuron decides to fire is not completely understood. Every neuron can receive signals from other brain cells through its dendrites. Some of these excite the neuron, pushing it closer to firing, while others calm it down. A dendrite can add up all the signals it receives, both calming and exciting, and pass the sum on to the cell body of its neuron. The neuron then adds up all the signals from its dendrites and uses that sum to decide whether or not to fire. Thats the process that researchers still dont entirely understand. To research it, neuroscientists need methods for monitoring electrical signals in the thin dendritic branches. This video shows a new method using light to explore electrical signals in different compartments of a neuron simultaneously. The intensity of the light reveals the voltage in that section of the neuron:

The video shows three consecutive voltage waves (from three nerve impulses) spreading from a neurons cell body into its dendrites. The colors represent light intensity. The light intensity is proportional to the voltage on the surface of the neuron; black is the minimal intensity on this scale, and red is maximal intensity.

To track all those electrical signals, neuroscientists used to have to wire up tiny electrodes to thin dendritic branches. But that method is cumbersome and difficult.

More recently, neuroscientists have begun creating fluorescent proteins that make the neuron light up when it receives an electrical signal. Thats whats being shown in the video. These Genetically Encoded Voltage Indicators (GEVIs), have potential to improve our ability to record voltages in neurons. This is what the glow looks like from many neurons fluorescing at the same time:

UConn School of Medicine neuroscientist Srdjan Antic and his colleagues noticed that many GEVIs have been invented, but few people use them. So they obtained as many GEVIs as possible and tested them in three separate ways, and reported the results in eNeuro on 08 September 2020.

First they tested the GEVIs in neurons cultured in a dish. They were able to detect single nerve impulses optically, but the cultured neurons were too variable to be used for systematic comparisons between the GEVIs.

So then they tested the GEVIs in non-neurons, cells called HEK293 cells. These cells are big, grow well in a dish, and were uniform enough to compare GEVIs:

Finally, the Antic lab expressed the GEVIs in animal brains and compared how various GEVIs did in groups of cells.

They found that all the GEVIs worked pretty well, and were easy to seein large populations of cells. The next step will be to test them in individual neurons, and perhaps even individual dendrites. Because when it comes to information processing in the brain,the most interesting things happen in dendrites, says Antic, associate professor of neuroscience at UConns medical school

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Testing the Fluorescent Proteins That Light Up the Brain - UConn Today

Neuroscience

The protein Klotho could extend the life of the brain. Is that a good thing? – Massive Science

Now's the time to live forever. Futurologists and transhumanists are poking themselves with what molecules they can, seeing what there is that might extend their lives or preserve their brains. One of the most intriguing molecules out there is called Klotho. Identified in 1997, it's named for the Fate of ancient Greek mythology who spun the thread the life. Mice that have a severely limited amount of Klotho in their body age rapidly and die prematurely. On the other hand, mice that carry more Klotho than normal live longer lives and appear to be resistant in some ways to aging.

Last April, an article appeared in the New York Times, titled "One Day There May Be a Drug to Turbocharge the Brain. Who Should Get it?" Massive contributor and neuroscientist Yewande Pearse and editor Dan Samorodnitsky sat down (in front of their computers) to talk about Klotho what it is, what it does, and whether prescribing a drug to supercharge the brain is a good idea.

Dan Samorodnitsky: Would it have to be prescribed by a doctor? Bought over the counter? Available at *chuckles to self* "Klotho shops"?

Yewande Pearse: This is a really interesting question because unlike a lot of other drugs, Klotho is a) a naturally occurring protein and b) has the potential to protect, treat and enhance the brain, therefore, the answer depends on the circumstances.

Mouse studies have revealed that Klotho plays an important role in the aging process. Mice with mutations in the Klotho gene have phenotypes which resemble different aspects of human aging, such as slowed growth, calcifying blood vessels, osteoporosis, and premature death. With respect to brain function, when mice with symptoms of age-related Alzheimer's disease are given Klotho, they are protected from cognitive decline. However, the exact biological function of Klotho and the way in which Klotho deficiency contributes to age-related diseases is not understood in mice, let alone humans.

Klotho has also has been shown to decrease with age in human blood serum samples, which may have something to do with cognitive decline in aging. Having said that, we all age, but we don't all develop Alzheimer's disease. Interestingly, people who carry a genetic variation of the Klotho gene that causes them to produce more Klotho, seem to not only be protected from Alzheimer's disease, but also perform better on cognitive tests like the Mini-Mental State Exam (MMSE)than people who produce average levels of Klotho.

Therefore, this becomes a question of dosage. To answer whether Klotho would have to be prescribed, we need to figure out the dose of Klotho required to prevent, treat, and enhance, and whether there are dose dependent risks. Perhaps a good starting point would be to calculate how much extra Klotho people with that gene variant produce compared to the average person versus how much less Klotho people who develop Alzheimer's disease have compared to those who do not of the same age.

It is also important to think about the structure and expression of Klotho when answering this question. Klotho is actually a transmembrane protein which means that it sits in the cell wall. Most of Klotho exists outside of the cell, but can be chopped off and released into the blood, urine, and cerebrospinal fluid. These different forms of Klotho all have different functions. Therefore, simply taking Klotho orally, is not as simple as it sounds, as it is unlikely that it will get it into its natural place in thebody, especially if we are trying to get it to the brain where it would have to cross the blood-brain-barrier, which prevents large molecules from passing through. To properly capture the full range of Klotho functions, we may be better off thinking about targeting the gene expression of Klotho itself something that may go beyond even a doctors prescription.

Multi-color whole brain image taken by fMRI

NIH via Flickr

But are naturally occurring levels of Klotho at the evolutionarily "correct" expression level?

Klotho is considered to be an aging-suppressor gene with multiple functions that protect organs. However, this protection doesn't last forever as Klotho declines with age.

To answer this question, we need to address a different question first: How and why do we age? There is no unified theory to explain the overall transformation taking place in the body during aging, but several theories, such as random mutation of genes, accumulation of damage by free radicals and the degeneration of functions like immunity are all valid on a local level. The reduction in Klotho as we age, for example, might fall into the last category, helping to explain dementia in the aging brain.

The "why?" is about trying to understand aging in terms of its necessity for survival. That sounds like a contradiction but is important when considering whether or not we should be taking Klotho as a drug. In 1889, August Weismann proposed that aging is a natural process of wearing out. If this is the case, then it is tempting to argue that there is no evolutionarily "correct" expression level of Klotho beyond child-bearing age. Klotho protects us for long enough to pass on our genes, after which point evolution has no reason to select for prolonged lifespan. This is why we don't all carry the "extra Klotho" genetic variant. However, the fact that better health care has granted us longer life regardless means that having higher levels of Klotho to maintain cognition is certainly preferable, and we could also argue that naturally occurring levels of Klotho are inadequate and should be augmented. Does that make sense?

It does make sense. Should we be concerned about, I don't know how to put it, over-correction? It feels like a moving target to nail down a dosage of Klotho that works well with any individual's natural expression of Klotho, natural variants, mutations, the three different variants of Klotho, just the overall difficulty of nailing down medications aimed at the nervous system.

Definitely, I think that caution is certainly needed given the fact that some studies have shown that one variant is actually associated with increased dementia and schizophrenia, suggesting that positive effects of Klotho on cognition may actually be limited by time, sex, and other factors. Having said that, all drugs, many of which have saved and improved lives, face the same challenge.

I think that Klotho research should focus on preventing the development of Alzheimers in people at risk first. In other words, trying to better understand Klotho as a potential biomarker, not just a treatment. There are no human studies to show what happens when Klotho is given to those who already have dementia, so early intervention is probably key. For the rest of us, research should focus on how our natural expression level of Klotho might be impacted by diet, exercise, etc., rather than heading straight down the pharmaceutical rout. For example, studies show that exercise, carbs, activated charcoal, probiotics and even statins can all increase the production of Klotho.

Is there evidence of disease from lack of Klotho in the body (maybe similar to imbalances occurring in some mental illnesses)?

The first clues about the function of Klotho came from mouse studies in which, the Klotho gene was deliberately mutated so that they didn't produce the normal level of Klotho. These mice had shorter life-spans and interestingly, showed a rapid decline in cognitive function, but only after a certain age. With mouse studies continuing to support the idea that Klotho expression levels correlate with both body (Klotho is made in the kidney too!) and brain function, there is now a lot of interest in Klotho as an indicator of health and disease.

A lack of Klotho in the body has been shown to correlate with a number of psychological conditions from chronic stress, which can lead to other psychiatric illnesses, and bipolar disorder. Lower levels of Klotho have also been associated with disease severity in multiple sclerosis and epilepsy. Generally, Klotho levels are lower in older people, but in Alzheimer's disease, patients, especially female patients, have even less Klotho.

A cross-section of a mouse cerebellum

NIH via Flickr

Also, and I'm sorry to keep harping on this, there's this quote from the original New York Times article that started this conversation:

"Some people carry a genetic variation that causes them to produce higher levels of Klotho than average in their bodies. Dr. Dubal and her colleagues identified a group of healthy old people with the variant and tested their cognition.

They scored better than people who make an average level of Klotho. Its not like they didnt undergo cognitive decline, said Dr. Dubal. Its just that they started off higher.

Maybe I'm just confused about the difference between Klotho making people "smarter" and people having "higher cognition" or something?

This is the part of the article that really jumped out at me. This is an important distinction. In this study, they found that differences in cognition as measured by IQ scores were only apparent after the age of 60. This means that these individuals experienced a delay in cognitive decline compared to people of the same age with the normal level of Klotho. Before 60, IQ scores were comparable but then after 60, people with lower levels of Klotho experienced a drop in IQ. Klotho is all about anti-aging, so we need to thinking about cognitive decline as a feature of aging and Klotho as an anti-aging protein. Assuming that we have the same IQ and we don't have the Klotho variant, if you were to start taking Klotho now (pretend they've cracked the issues above) and I didn't, I don't think you'd suddenly get smarter, I just think that when we got older, I'd start experiencing cognitive decline before you.

Do you worry about the number of apparent medical functions Klotho has ascribed to it? Increases overall brain function (but doesn't make you smarter), increases lifespan, and protects against a bunch of different, un-related diseases like Alzheimer's, Parkinson's, and MS? Seems like a lot of effects for one protein.

I am fascinated by the fact that Klotho has so many effects! It's a bit of a super protein. I am not surprised though because although all these effects seem disparate, they share common pathways upon which Klotho acts. For example, Kotho has antioxidant effects that are important for multiple functions both in the brain and the kidneys.

What I am worried about though is the fact that little is actually known about the function of Klotho and how aging suppression might work. I think we should be very careful about altering something that does indeed have so many actions and effects. Once Klotho is secreted, it enters the blood stream and goes everywhere, but by taking Klotho orally, I am not sure how can we ensure Klotho is going to the right places in the right quantities in a way that is effective and safe.

Do you worry about the ethics of taking Klotho? Taking it as a replacement drug, like if someone has low Klotho, seems fine, but beyond that? Should neuroscience researchers worry about that?

Are you asking me whether I think it's unethical to want to live longer and better? I'm tempted to go off on a tangent about our human endeavor to live forever and what that is doing to the environment. But, if we are going to live longer, is it wrong to want a better quality of life as measured by staying sharper into out 70s, 80s and 90s? I don't think that desire is unethical.

However, if we are talking about the ethics of taking an enhancement drug that not everyone has access to then my answer would lean more towards no but I'd say the same about food equity and a hundred other things that influence our health and well-being. I guess that answer is more personal. As a neuroscience researcher, my priority is safety and the ethics around that. If we can ensure that taking "extra" Klotho is safe and effective then, I don't think we should be worried. I mean, I can't speak for neuroscientists everywhere, but if some of us are willing to research how zapping the brains of healthy adults to improve memory and potentially improve cognitive function, then relatively speaking, I don't think researching the additive effects of a naturally occurring protein is a concern.

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The protein Klotho could extend the life of the brain. Is that a good thing? - Massive Science

Neuroscience

Opinion: Scientists have failed to convey findings effectively – The Cincinnati Enquirer

Christin Godale, Opinion contributor Published 10:15 a.m. ET Oct. 19, 2020

(Photo: Getty Images)

In the depths of pursuing a Ph.D. in neuroscience, I spend most of my time in a dark, windowless room using a microscope to take pictures of brain cells. When I do emerge from behind my microscope, I rarely discuss my research with other people, frankly because, like many other early-career scientists, I have not been adequately trained in communicating my research with the public. The COVID-19 pandemic has dramatically changed this dynamic; however, scientists are now encouraged, expected, and even required to explain what is happening across the country.

The "new normal"that we live in poses quite a dilemma to the scientific community. Researchers, like myself, perform experiments and collect and analyze data within academic contexts. We are taught to acknowledge our experiments shortcomings and propose innovative approaches in our grants and peer-reviewed papers. As a result, scientists are open to change whether that is changing a predictive model because of new data or redesigning an experiment because they thought of a new and better approach. Now, scientists need to adapt to the changing conditions outside the lab and seek better ways to communicate science to the public and, as a scientist, I am no different.

Throughout my eight years of combined undergraduate and graduate education, public communication has never been part of the curriculum. Many rising early-career scientists, including myself, believe our field must learn to clearly and effectively communicate our research to the taxpayers that fund it. Yet, it is often challenging to translate complex scientific concepts filled with jargon into clear, concise terms and ideas that the public can thoughtfully digest.

Scientist looking at a digital rendering of a coronavirus(Photo: Getty Images)

But there is good news! Many scientists across the nation are trying to find ways to develop their science communication skills. Professional societies like the Society for Neuroscience, the American Association for the Advancement of Science, and The National Academies of Science have developed an extensive collection of tools and programs, like science communication courses and science policy fellowships to help scientists create the necessary skillset to communicate with you, the public. Locally, the University of Cincinnati offers science communication classes. I plan to enroll in one or two of these lectures because I owe it to you as a scientist and as a community member to improve my skills.

The scientific community should have learned lessons from the last pandemic in 1918 that science communication was critical to stifling misinformation. Instead, we are seeing the same missteps today as COVID-19 misinformation circulates on various websites and social media platforms. Much of this pandemic misinformation stems from focusing on single-study results without context; overemphasizing results, particularly treatment effects, without considering limitations; and communicating results that have not been peer-reviewed by the scientific community.

(Photo: Getty Images)

Still, there are a lot of trustworthy resources that you can use to learn about COVID-19s biology, transmission, symptoms, and how to protect yourself, your family, and your community from the coronavirus. I recommend using The Federation of American Scientists COVID-19 question resource (covid19.fas.org), which is designed to connect public members with scientists trained in science communication to answer any and every question you might have about COVID-19.

As scientists, our purpose is to stretch the bounds of human knowledge, but at times, we have failed to communicate our findings with the public effectively. Now we have to take a step back and acknowledge the gaps in our education and work to improve our science communication skills. Science is a powerful tool, but it is up to every individual scientist to become a communicator and ensure our work contributes to solving societal problems instead of making them worse.

Christin Godale is a Neuroscience Doctoral Candidate at the University of Cincinnati College of Medicine and the former Graduate Student Trustee on the University of Cincinnati Board of Trustees.

Christin Godale(Photo: Provided)

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Opinion: Scientists have failed to convey findings effectively - The Cincinnati Enquirer

Neuroscience

Tim Chucks Cole, one half of The Correspondents, has died aged 35 – NME

Tim Cole, who performed as DJ Chucks in British electronic duo The Correspondents, died over the weekend, aged 35.

According to a Facebook post overnight from bandmate Ian Bruce (aka Mr Bruce), Cole passed away last Sunday (October 18). No cause of death was revealed.

He was a brilliant, complicated man who never fully appreciated the extent of his own talent. Hes the reason I bounced around like a lunatic for 13 years, Bruce said on Facebook.

And in a funny kind of way hes the reason the band lasted so long as he always chose integrity over hype, he was a facts not fads kinda guy.

I will miss his wit and cynicism. Him trying to explain neuroscience to me. I guess I will even miss having to sit through hours of cricket commentary on long car journeys to festivals.

Im devastated to inform you all that my band mate Tim Cole (aka Chucks) unexpectedly died last Sunday. We are all in

Posted by The Correspondents onTuesday, October 20, 2020

Cole and Bruce formed The Correspondents in 2007. Over the course of 13 years, the duo released two albums and a handful of EPs, and were on the lineups of Glastonbury, Bestival and WOMAD. Their last release was their 2019 EP, Who Knew.

Life on the road with endless gigs, airports, hotels and soundchecks took its toll, Bruce said, But the sense of achievement and satisfaction after each show was something palpable that we would always share and enjoy.

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Tim Chucks Cole, one half of The Correspondents, has died aged 35 - NME

Neuroscience

Why We Lie, And The Neuroscience Behind It – Forbes

Shutterstock

Im fine.

Of course I love you.

Ill call you.

No, you dont look fat in those jeans.

We are liars.

All of us.

We lie to save face, to avoid hurting other peoples feelings, to impress others, to shirk responsibility, to hide misdeeds, as a social lubricant, to prevent conflict, to get out of work, and many more reasons.

And we lie a lot.

Deception costs businesses and government billions, ruins relationships, undermines what we care about and even takes lives. The more white matter (see my blog The Truth About How Your Brain Gets Smarter)or some might even say the more intelligent the neocortexthe greater potential a person has to lie.

Bella DePaulo, Ph.D., a psychologist at the University of Virginia, has confirmed that lying is simply a condition of life. In her research she found that both men and women lie in approximately a fifth of their social exchanges lasting 10 or more minutes. Wow. And over the course of a week we deceive about 30 percent of people we have 1:1 interactions with. Wow wow.

Women are more likely to tell altruistic lies to avoiding hurting other peoples feelings, and men are more likely to lie about themselves. De Paulo found that men lie more often to impress. A typical conversation between two guys contains about eight times as many self-oriented lies as it does lies about others.

Your Brain On Lies

Three key parts of our brain are stimulated when we lie. First, the frontal lobe (of the neocortex), which has the ability to suppress truthyes, its capable of dishonesty due to its intellectual role. Second, the limbic system due to the anxiety (hi, amygdala!) that comes with deceptionand yes, when were lied to our Spiderman sense here can perk up, just as we can feel guilty/stressed when were doing the lying. And third, the temporal lobe is involved because its responsible for retrieving memories and creating mental imagery. Just for fun, add the anterior cingulate cortex because it helps in monitoring errors, and the dorsal lateral prefrontal cortex because it is trying all the while to control our behavior. Our brain is busy, busy, busy when we lie.

And its far more peaceful when we tell the truth, because our limbic systems isnt stressed about lying and our frontal lobe isnt inhibiting the truth.

Lies At Work

Where do we see a prevalence of lies? At work, or more specifically, to get out of work.

According to Zetys recent 2020 research, of over 1,000 Americans, they found 96% confessed to lying to get out of work. Heres the net-net:

More men than women were caught lying, and only 27% of respondents who lied to get out of work regretted it. For those caught, 70% regretted lying. But despite not feeling bad about themselves for lying, 59% of respondents said they wouldnt do it again.

Heres a silver lining: the older we get, the less compelled we are to lie to avoid work. Zety found:

Zety

Are we all pathological liars? Or do we need to look at why we feel compelled to make up stories instead of just telling the truth? Is lying to avoid work a cultural problem, at least in part? And what about people that dont experience regret when they lie? The stance of perpetual innocence, or extreme entitlement (and thus reality distortion) is a topic I addressed in my blogs on Borderline Personalities: How To Survive and How To Thrive.

Lying Rx

To reduce the amount of lying in your workplace, youll want to first look at how safe people feel. Is it ok to tell the truth? Is it ok to fail? Is it ok to be human and not a super hero/work robot/cog in a wheel? Is it ok to have feelings and need a break now and then? Find out.

Do regular employee engagement surveys see our fave one here.

Use the emotion wheel at the beginning of each meeting to check in on how everyone is doing

Create support groups if people need a little extra help

So why do we lie? Because it works for us. Temporarily, at least. For fun, you might want to join me in telling the five types of truth; youll notice not only how good it feels, but how much simpler it makes your life.

How often do you lie? Why?

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Why We Lie, And The Neuroscience Behind It - Forbes

Neuroscience

Neuroscience Can Help Us Understand Why Free Will Is Real – Walter Bradley Center for Natural and Artificial Intelligence

Evolutionary biologist Jerry Coyne seems obsessed with denying free will. In a recent post on his blog, Why Evolution Is True, he supported the claim of theoretical physicist Sabine Hossenfelder that we do not have free will:

If youve read this site, youll know that my own views are pretty much the same as hers, at least about free will. We dont have it, and the fundamental indeterminacy of quantum mechanics doesnt give it to us either.

Hossenfelder doesnt pull any punches:

This means in a nutshell that the whole story of the universe in every single detail was determined already at the big bang. We are just watching it play out.

QED!

Both Coyne and Hossenfelder are atheists, materialists, and deterministsa sort of intellectual dark triadand their beliefs are scientifically and logically uninformed. They use denial of free will to prop up their materialist and determinist irreligion. It is not science; it is an ideological project, without a shred of science or logic to back it up.

There are three lines of evidence supporting the reality of free will: Neuroscience, physics and philosophy all point to the fact that free will is real. In this post, Ill discuss the neuroscience. But first, we must start by understanding what free will is. Erroneous definition of free will is at the root of many mistakes inherent in denying it.

It turns out that free will is rather hard to define rigorously, if taken all by itself. Many have tried. Definitions such as choice that is uncaused, choice that is an inclination that originates wholly within an organism, and choice that entails the existence of alternative possibilities have been proposed. Each is inadequate to the situation.

The definition of free will really depends on the definition of will. Will is a subset of appetite (an Aristotelian term), which means an inclination to act. There are two kinds of appetitesensitive appetite and rational appetite. Sensitive appetites are appetites that arise from concrete perceptions and imagination. I perceive a piece of cake, and I imagine how wonderful it would taste, so (if I am impulsive) I eat it.

Rational appetite is inclination to act based on reason, not on perceptions or imagination. Suppose, for example, that I am on a diet. My decision about whether to eat a piece of cake because of its appearance and how I imagine it will taste is fundamentally different from my decision about whether I will break my diet in order to do so. One inclinationmy sensitive appetiteis based on concrete perception. The other inclinationto follow my dietis based on abstract reason.

Only abstract reason/rational appetite is the will part of free will. Sensitive appetite is not part of the willit is a passion based wholly on material factorsmy brain chemistry, etc. Sensitive appetite is not freethis kind of appetite is indeed dictated by my molecules and neurotransmitters. I can condition it and override it but in itself, it is wholly material and subject to the laws of nature.

My willmy rational appetiteis an immaterial power of my mind. My will can be influenced by my passions but it is inherently free of material determinism of any kind. For example, my decision whether or not to eat that piece of cake is the result of the struggle between my material passions and my immaterial willbetween my sensitive and my rational appetite. Sometimes my passion wins. Sometimes my reasonmy willwins.

Now that we have a satisfactory definition of will, what do we mean by free will? Philosopher and theologian Thomas Aquinas gave the best answer: My free will is inclination based on abstract reasoning that arises wholly from me. Nothing other than me determines my will. I determine my will and my will is an immaterial power of my soul. In this specific sense, I have free will.

Now lets get to the neuroscience. Neuroscience has a lot to contribute to the debate over free will and all of it supports the reality of free will. There isnt a shred of neuroscientific evidence that contradicts the reality of free will.

Two major types of experiments address the question of free will:

The first is the experiments of Benjamin Libet, a mid- to late 20th century neuroscientist who studied the precise timing of electrical activity in the brain and conscious decisions to do simple tasks such pushing a button. Libet found that we have pre-conscious impulses characterized by spikes in brain waves that precede conscious decisions by about a half-second. But he also found that these pre-conscious impulses (which are not freely generated) are merely temptations. We retain the power to accept or reject them, and acceptance or rejection of these temptations is not accompanied by brain waves. Libet called this state free wont: We are bombarded by temptations that are beyond our immediate control but we have the immaterial freedom to accept or reject them. He noted the congruence between his experimental results and the traditional Jewish and Christian understanding of sin. We are tempted involuntarily but we always have freedom to comply with or reject temptation.

The second set of experiments is, in my view, even more compelling. They derive from the work of Wilder Penfield, the pioneer in the neurosurgery of epilepsy in the mid-20th century. Penfield performed over a thousand awake brain operations on patients with epilepsy. He stimulated their brains and the recorded the effect of stimulation on these awake patients. He found that he was able to stimulate practically any concrete mental phenomenonmovement of limbs, perceptions of light or smell or tactile sensations, emotions, memoriesbut he was never able to stimulate abstract thought or free will. In his memoir, Mystery of the Mind, he concluded that abstract thought and free will (which he called the mind as distinct from automatic responses like perceptions, movements, or emotions) did not originate in the brain, but were immaterial powers of the soul. He began his career as a strict materialist but ended his career as a convinced dualist.

He also noted a remarkable fact: there are no intellectual seizures, and by implication, no seizures that invoke free will. There are no calculus seizures, no logic seizures, no seizures that make the patients think abstractly or will (apparently) freely. There are no seizures that make you choose to be a Republican or a Democrat, no seizures that make you Christian or Jewish, no seizures that make you apply certain kinds of logic to a problem rather than another kind of logic. This is remarkable: if the will is merely the product of brain activity, at least some seizures should evoke will. They never do. Many seizures do feature complex manifestations (theyre called complex partial seizures), but these complex seizures always involve concrete thoughts and actions perceptions, emotions, and stereotypic movements. There are no seizures that invoke abstract thought or abstract decisionsthere are no free will seizures.

This remains true to this day. There are no reports in the medical literaturedespite literally billons of seizures suffered by patients in the modern eraof any seizure that replicates free will. This remarkable factliterally based on billions of data pointsclearly shows that the will is not determined by the material state of the brain. If the will were determined by neural activity, the willabstract choice based on reasonwould at least occasionally be replicated by seizures. It never is.

Coyne, Hossenfelder and other free will deniers are ignorant of the mountain of neuroscience evidence confirming free will. They are also ignorant of the philosophical reasoning supporting free will and of the evidence in physics that refutes determinism (but these are both subjects for another post).

If Dr. Coyne reads this far in this post, I challenge him: If free will is determined by brain states, show us the medical or neuroscience evidence that free will is ever evoked by seizure or by neurosurgical stimulation of the brain. In other words, Dr. Coyne, show me the neuroscience behind your bizarre denial of free will.

NeurosurgeonMichael Egnorhas written a fair bit on free will forMind Matters News.Here are some selections to consider:

No free will meansno justice:Free will is the cornerstone of all human rights and the cornerstone of our Constitutional rights. The denial of free will is, literally, the denial of human freedom. Without free will, we are livestock, without the presumption of innocence, without actual innocence, and without rights. A justice system that has no respect for free willa justice system in which human choices are diseases is a system of livestock management applied to homo sapiens.

Also:

Jerry Coyne just cant give updenying free will.Coynes denial of free will, based on determinism, is science denial and junk metaphysics

How Libets free will researchis misrepresented:Sometimes, says Michael Egnor, misrepresentation may be deliberate because Libets work doesnt support a materialist perspective.

Doesalien hand syndromeshow that we dont really have free will? One womans left hand seemed to have a mind of its own. Did it?

and

Does brain stimulation researchchallenge free will?If we can be forced to want something, is the will still free?

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Neuroscience Can Help Us Understand Why Free Will Is Real - Walter Bradley Center for Natural and Artificial Intelligence

Neuroscience

MRI and PET Reveal Link Between Blood Flow and Tau Accumulation in Alzheimer’s Patients – Diagnostic Imaging

There is a connection between impaired blood flow and the build-up of tau protein in patients who have Alzheimers disease, according to findings revealed on MRI and PET scans.

In a study published Oct. 12 in the Journal of Neuroscience, a team of investigators from the University of Southern California (USC) in Los Angeles shed more light onto the vascular component of Alzheimers, noting that their findings point to the potential of a combination treatment.

Our results demonstrate vascular-tau association across the [Alzheimers disease] spectrum and suggest that early vascular-tau associations are exacerbated in the presence of amyloid, consistent with a two-hit model of [Alzheimers disease] on cognition, said the team led by Daniel Albrecht, Ph.D., a neuroimaging research fellow. Combination treatments targeting vascular health, as well as amyloid- and tau levels, may preserve cognitive function more effectively than single-target therapies.

To date, the connection between vascular dysfunction and tau pathology and how it affects cognition has not been well understood. Still, there is a growing body of evidence that shows vascular dysfunction plays a large part in Alzheimers pathophysiology.

Like the proverbial chicken and egg, it remains unclear if impaired blood flow causes or is caused by errant protein building, they said, or if these two symptoms occur for unrelated reasons.

Related Content: FDA Approves First Radiopharmaceutical for Imaging Tau

To dig deeper into this connection, Albrechts team used MRI and PET scans to compare blood flow and tau build-up in older adults. They examined 68 patients from USC who ranged from having normal cognition to showing signs of mild cognitive impairment, as well as a validation group of 138 individuals with mild cognitive impairment or Alzheimers disease who were enrolled in the Alzheimers disease Neuroimaging Initiative. Alongside their MRI and PET scans, all patients completed neuropsychological testing and were assessed for executive brain function, attention, and memory.

Based on their analysis, the team discovered that spots in the brain with more significant tau build-up also had decreased blood flow. This was particularly apparent in the inferior temporal gyrus the area of the brain which typically experiences tau build-up in patients with Alzheimers disease. The team pointed out that this relationship also held true for the validation group.

The correlation between tau and vascular function was stronger in people with greater cognitive impairment and higher amyloid- levels, they said. It also appeared in more brain regions as the disease progressed in severity.

Consequently, Albrechts team said, their results suggest that targeting vascular function could be key to avoiding and treatment Alzheimers.

Results from the current study provide the first evidence of associations between elevated tau PET signal and vascular dysfunction, they said. Take together, combination treatments targeting vascular health, as well as amyloid- and tau levels, may be more effective in preserving cognitive function than single-target therapies.

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MRI and PET Reveal Link Between Blood Flow and Tau Accumulation in Alzheimer's Patients - Diagnostic Imaging

Neuroscience

Monkey study suggests that they, like humans, may have ‘self-domesticated’ – Science Codex

It's not a coincidence that dogs are cuter than wolves, or that goats at a petting zoo have shorter horns and friendlier demeanors than their wild ancestors. Scientists call this "domestication syndrome" -- the idea that breeding out aggression inadvertently leads to physical changes, including floppier ears, shorter muzzles and snouts, curlier tails, paler fur, smaller brains, and more.

The link appears to come from certain neural crest cells, present before birth and in newborns, that have a versatility akin to stem cells. These neural crest cells can turn into a handful of different things, specifically adrenal cells -- which boost the strength of the "fight or flight" response -- as well as physical traits like larger teeth and stiffer ears.

Ever since Darwin's time, some scientists have speculated that humans "self-domesticated" -- that we chose less aggressive and more helpful partners, with the result that we have shifted the trajectory of our own evolution.

"The evidence for this has been largely circumstantial," said Asif Ghazanfar, a professor of psychology and neuroscience. "It's really a popular and exciting idea but one that lacks direct evidence, a link between friendly behavior and other features of domestication."

To see if the story could be put on a robust foundation, Ghazanfar turned to marmoset monkeys. Like humans, marmosets are extremely social and cooperative, plus they have several of the physical markers consistent with domestication, including a patch of white fur on their foreheads that is common in domesticated mammals.

What does cooperation look like in a monkey? Friendly vocal exchanges, caring for each other's young, and sharing food, among other signs, said Ghazanfar.

The research team showed that the size of a marmoset's white fur patch was strongly related to how frequently it produced friendly vocal responses to another. This is the first set of data to show an association between a friendly behavior and a physical domestication trait in individual animals.

To show a causal link between the white patch and vocal behavior, the researchers tested infant twins in different ways. In very brief sessions, one twin got reliable vocal feedback from a simulated parent -- a computer programmed with adult calls that responded to 100% of their vocalizations -- while the other twin only heard parental responses to 10% of their sounds.

These experimental sessions lasted 40 minutes, every other day, for most of the first 60 days of the monkeys' lives. For the other 23+ hours of each day, the monkeys were with their families.

In previous work, Ghazanfar and his colleagues showed that the infants who received more feedback learned to speak -- or more precisely, developed their adult-sounding calls -- faster than their siblings. By also measuring the white fur patches on the developing monkeys' foreheads at the same time and for three more months, the researchers discovered that the rate of the white facial coloration development was also accelerated by increased parental vocal responses. This shows a developmental connection between facial fur coloration and vocal development -- they are both influenced by parents.

That connection may be via those neural crest cells that can turn into "fight or flight" cells and that also contribute to parts of the larynx, which is necessary for producing vocalizations.

Domestication in other species has also been linked to changes in vocal behavior. Foxes selected for tameness have altered their vocalizations in response to the presence of humans. Similarly, a tame Bengalese finch learns and produces a more complex song, and retains greater song plasticity in adulthood, than its wild cousins.

But this is the first study linking the degree of a social trait with the size of a physical sign of domestication, in any species, said the researchers. Their findings are detailed in an article published online in the journal Current Biology. Ghazanfar's co-authors include Daniel Takahashi, a former postdoctoral researcher who is now a professor of neuroscience at Federal University of Rio Grande do Norte, Brazil; Rebecca Terrett of the Class of 2016; Lauren Kelly, Ghazanfar's former lab manager, who now works at Rutgers-Robert Wood Johnson Medical School; and two collaborators from New York University, James Higham and Sandra Winters.

"If you change the rate of the marmosets' vocal development, then you change the rate of fur coloration," said Ghazanfar. "It's both a fascinating and strange set of results!"

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Monkey study suggests that they, like humans, may have 'self-domesticated' - Science Codex

Neuroscience

tDCS, tACS and tRNS Market 2020 Outlook, Key Strategies, Manufacturers, Type and Application, Forecast To 2026 | Neuroelectrics, Magstim, NeuroCare…

The report titled Global tDCS, tACS and tRNS Market is one of the most comprehensive and important additions to QY Researchs archive of market research studies. It offers detailed research and analysis of key aspects of the global tDCS, tACS and tRNS market. The market analysts authoring this report have provided in-depth information on leading growth drivers, restraints, challenges, trends, and opportunities to offer a complete analysis of the global tDCS, tACS and tRNS market. Market participants can use the analysis on market dynamics to plan effective growth strategies and prepare for future challenges beforehand. Each trend of the global tDCS, tACS and tRNS market is carefully analyzed and researched about by the market analysts.The market analysts and researchers have done extensive analysis of the global tDCS, tACS and tRNS market with the help of research methodologies such as PESTLE and Porters Five Forces analysis. They have provided accurate and reliable market data and useful recommendations with an aim to help the players gain an insight into the overall present and future market scenario. The tDCS, tACS and tRNS report comprises in-depth study of the potential segments including product type, application, and end user and their contribution to the overall market size.

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In addition, market revenues based on region and country are provided in the tDCS, tACS and tRNS report. The authors of the report have also shed light on the common business tactics adopted by players. The leading players of the global tDCS, tACS and tRNS market and their complete profiles are included in the report. Besides that, investment opportunities, recommendations, and trends that are trending at present in the global tDCS, tACS and tRNS market are mapped by the report. With the help of this report, the key players of the global tDCS, tACS and tRNS market will be able to make sound decisions and plan their strategies accordingly to stay ahead of the curve.

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Key Players Mentioned in the Global tDCS, tACS and tRNS Market Research Report: Neuroelectrics, Magstim, NeuroCare Group, Soterix Medical, Newronika, Rogue Resolutions, Flow Neuroscience, Shenzhen Yingchi Technology, Shenzhen Hanix United, TCT Research, EB Neuro SpA

Global tDCS, tACS and tRNS Market Segmentation by Product: Transcranial Direct Current Stimulation (tDCS)Transcranial Alternating Current Stimulation (tACS)Transcranial Random Noise Stimulation (tRNS)

Global tDCS, tACS and tRNS Market Segmentation by Application: HospitalClinicHomeOthers

The tDCS, tACS and tRNS Market report has been segregated based on distinct categories, such as product type, application, end user, and region. Each and every segment is evaluated on the basis of CAGR, share, and growth potential. In the regional analysis, the report highlights the prospective region, which is estimated to generate opportunities in the global tDCS, tACS and tRNS market in the forthcoming years. This segmental analysis will surely turn out to be a useful tool for the readers, stakeholders, and market participants to get a complete picture of the global tDCS, tACS and tRNS market and its potential to grow in the years to come.

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Table of Contents:

1 tDCS, tACS and tRNS Market Overview1.1 Product Overview and Scope of tDCS, tACS and tRNS1.2 tDCS, tACS and tRNS Segment by Type1.2.1 Global tDCS, tACS and tRNS Production Growth Rate Comparison by Type 2020 VS 20261.2.2 Transcranial Direct Current Stimulation (tDCS)1.2.3 Transcranial Alternating Current Stimulation (tACS)1.2.4 Transcranial Random Noise Stimulation (tRNS)1.3 tDCS, tACS and tRNS Segment by Application1.3.1 tDCS, tACS and tRNS Consumption Comparison by Application: 2020 VS 20261.3.2 Hospital1.3.3 Clinic1.3.4 Home1.3.5 Others1.4 Global tDCS, tACS and tRNS Market by Region1.4.1 Global tDCS, tACS and tRNS Market Size Estimates and Forecasts by Region: 2020 VS 20261.4.2 North America Estimates and Forecasts (2015-2026)1.4.3 Europe Estimates and Forecasts (2015-2026)1.4.4 China Estimates and Forecasts (2015-2026)1.4.5 Japan Estimates and Forecasts (2015-2026)1.5 Global tDCS, tACS and tRNS Growth Prospects1.5.1 Global tDCS, tACS and tRNS Revenue Estimates and Forecasts (2015-2026)1.5.2 Global tDCS, tACS and tRNS Production Capacity Estimates and Forecasts (2015-2026)1.5.3 Global tDCS, tACS and tRNS Production Estimates and Forecasts (2015-2026)1.6 tDCS, tACS and tRNS Industry1.7 tDCS, tACS and tRNS Market Trends

2 Market Competition by Manufacturers2.1 Global tDCS, tACS and tRNS Production Capacity Market Share by Manufacturers (2015-2020)2.2 Global tDCS, tACS and tRNS Revenue Share by Manufacturers (2015-2020)2.3 Market Share by Company Type (Tier 1, Tier 2 and Tier 3)2.4 Global tDCS, tACS and tRNS Average Price by Manufacturers (2015-2020)2.5 Manufacturers tDCS, tACS and tRNS Production Sites, Area Served, Product Types2.6 tDCS, tACS and tRNS Market Competitive Situation and Trends2.6.1 tDCS, tACS and tRNS Market Concentration Rate2.6.2 Global Top 3 and Top 5 Players Market Share by Revenue2.6.3 Mergers & Acquisitions, Expansion

3 Production and Capacity by Region3.1 Global Production Capacity of tDCS, tACS and tRNS Market Share by Regions (2015-2020)3.2 Global tDCS, tACS and tRNS Revenue Market Share by Regions (2015-2020)3.3 Global tDCS, tACS and tRNS Production Capacity, Revenue, Price and Gross Margin (2015-2020)3.4 North America tDCS, tACS and tRNS Production3.4.1 North America tDCS, tACS and tRNS Production Growth Rate (2015-2020)3.4.2 North America tDCS, tACS and tRNS Production Capacity, Revenue, Price and Gross Margin (2015-2020)3.5 Europe tDCS, tACS and tRNS Production3.5.1 Europe tDCS, tACS and tRNS Production Growth Rate (2015-2020)3.5.2 Europe tDCS, tACS and tRNS Production Capacity, Revenue, Price and Gross Margin (2015-2020)3.6 China tDCS, tACS and tRNS Production3.6.1 China tDCS, tACS and tRNS Production Growth Rate (2015-2020)3.6.2 China tDCS, tACS and tRNS Production Capacity, Revenue, Price and Gross Margin (2015-2020)3.7 Japan tDCS, tACS and tRNS Production3.7.1 Japan tDCS, tACS and tRNS Production Growth Rate (2015-2020)3.7.2 Japan tDCS, tACS and tRNS Production Capacity, Revenue, Price and Gross Margin (2015-2020)

4 Global tDCS, tACS and tRNS Consumption by Regions4.1 Global tDCS, tACS and tRNS Consumption by Regions4.1.1 Global tDCS, tACS and tRNS Consumption by Region4.1.2 Global tDCS, tACS and tRNS Consumption Market Share by Region4.2 North America4.2.1 North America tDCS, tACS and tRNS Consumption by Countries4.2.2 U.S.4.2.3 Canada4.3 Europe4.3.1 Europe tDCS, tACS and tRNS Consumption by Countries4.3.2 Germany4.3.3 France4.3.4 U.K.4.3.5 Italy4.3.6 Russia4.4 Asia Pacific4.4.1 Asia Pacific tDCS, tACS and tRNS Consumption by Region4.4.2 China4.4.3 Japan4.4.4 South Korea4.4.5 Taiwan4.4.6 Southeast Asia4.4.7 India4.4.8 Australia4.5 Latin America4.5.1 Latin America tDCS, tACS and tRNS Consumption by Countries4.5.2 Mexico4.5.3 Brazil

5 tDCS, tACS and tRNS Production, Revenue, Price Trend by Type5.1 Global tDCS, tACS and tRNS Production Market Share by Type (2015-2020)5.2 Global tDCS, tACS and tRNS Revenue Market Share by Type (2015-2020)5.3 Global tDCS, tACS and tRNS Price by Type (2015-2020)5.4 Global tDCS, tACS and tRNS Market Share by Price Tier (2015-2020): Low-End, Mid-Range and High-End

6 Global tDCS, tACS and tRNS Market Analysis by Application6.1 Global tDCS, tACS and tRNS Consumption Market Share by Application (2015-2020)6.2 Global tDCS, tACS and tRNS Consumption Growth Rate by Application (2015-2020)

7 Company Profiles and Key Figures in tDCS, tACS and tRNS Business7.1 Neuroelectrics7.1.1 Neuroelectrics tDCS, tACS and tRNS Production Sites and Area Served7.1.2 Neuroelectrics tDCS, tACS and tRNS Product Introduction, Application and Specification7.1.3 Neuroelectrics tDCS, tACS and tRNS Production Capacity, Revenue, Price and Gross Margin (2015-2020)7.1.4 Neuroelectrics Main Business and Markets Served7.2 Magstim7.2.1 Magstim tDCS, tACS and tRNS Production Sites and Area Served7.2.2 Magstim tDCS, tACS and tRNS Product Introduction, Application and Specification7.2.3 Magstim tDCS, tACS and tRNS Production Capacity, Revenue, Price and Gross Margin (2015-2020)7.2.4 Magstim Main Business and Markets Served7.3 NeuroCare Group7.3.1 NeuroCare Group tDCS, tACS and tRNS Production Sites and Area Served7.3.2 NeuroCare Group tDCS, tACS and tRNS Product Introduction, Application and Specification7.3.3 NeuroCare Group tDCS, tACS and tRNS Production Capacity, Revenue, Price and Gross Margin (2015-2020)7.3.4 NeuroCare Group Main Business and Markets Served7.4 Soterix Medical7.4.1 Soterix Medical tDCS, tACS and tRNS Production Sites and Area Served7.4.2 Soterix Medical tDCS, tACS and tRNS Product Introduction, Application and Specification7.4.3 Soterix Medical tDCS, tACS and tRNS Production Capacity, Revenue, Price and Gross Margin (2015-2020)7.4.4 Soterix Medical Main Business and Markets Served7.5 Newronika7.5.1 Newronika tDCS, tACS and tRNS Production Sites and Area Served7.5.2 Newronika tDCS, tACS and tRNS Product Introduction, Application and Specification7.5.3 Newronika tDCS, tACS and tRNS Production Capacity, Revenue, Price and Gross Margin (2015-2020)7.5.4 Newronika Main Business and Markets Served7.6 Rogue Resolutions7.6.1 Rogue Resolutions tDCS, tACS and tRNS Production Sites and Area Served7.6.2 Rogue Resolutions tDCS, tACS and tRNS Product Introduction, Application and Specification7.6.3 Rogue Resolutions tDCS, tACS and tRNS Production Capacity, Revenue, Price and Gross Margin (2015-2020)7.6.4 Rogue Resolutions Main Business and Markets Served7.7 Flow Neuroscience7.7.1 Flow Neuroscience tDCS, tACS and tRNS Production Sites and Area Served7.7.2 Flow Neuroscience tDCS, tACS and tRNS Product Introduction, Application and Specification7.7.3 Flow Neuroscience tDCS, tACS and tRNS Production Capacity, Revenue, Price and Gross Margin (2015-2020)7.7.4 Flow Neuroscience Main Business and Markets Served7.8 Shenzhen Yingchi Technology7.8.1 Shenzhen Yingchi Technology tDCS, tACS and tRNS Production Sites and Area Served7.8.2 Shenzhen Yingchi Technology tDCS, tACS and tRNS Product Introduction, Application and Specification7.8.3 Shenzhen Yingchi Technology tDCS, tACS and tRNS Production Capacity, Revenue, Price and Gross Margin (2015-2020)7.8.4 Shenzhen Yingchi Technology Main Business and Markets Served7.9 Shenzhen Hanix United7.9.1 Shenzhen Hanix United tDCS, tACS and tRNS Production Sites and Area Served7.9.2 Shenzhen Hanix United tDCS, tACS and tRNS Product Introduction, Application and Specification7.9.3 Shenzhen Hanix United tDCS, tACS and tRNS Production Capacity, Revenue, Price and Gross Margin (2015-2020)7.9.4 Shenzhen Hanix United Main Business and Markets Served7.10 TCT Research7.10.1 TCT Research tDCS, tACS and tRNS Production Sites and Area Served7.10.2 TCT Research tDCS, tACS and tRNS Product Introduction, Application and Specification7.10.3 TCT Research tDCS, tACS and tRNS Production Capacity, Revenue, Price and Gross Margin (2015-2020)7.10.4 TCT Research Main Business and Markets Served7.11 EB Neuro SpA7.11.1 EB Neuro SpA tDCS, tACS and tRNS Production Sites and Area Served7.11.2 EB Neuro SpA tDCS, tACS and tRNS Product Introduction, Application and Specification7.11.3 EB Neuro SpA tDCS, tACS and tRNS Production Capacity, Revenue, Price and Gross Margin (2015-2020)7.11.4 EB Neuro SpA Main Business and Markets Served

8 tDCS, tACS and tRNS Manufacturing Cost Analysis8.1 tDCS, tACS and tRNS Key Raw Materials Analysis8.1.1 Key Raw Materials8.1.2 Key Raw Materials Price Trend8.1.3 Key Suppliers of Raw Materials8.2 Proportion of Manufacturing Cost Structure8.3 Manufacturing Process Analysis of tDCS, tACS and tRNS8.4 tDCS, tACS and tRNS Industrial Chain Analysis

9 Marketing Channel, Distributors and Customers9.1 Marketing Channel9.2 tDCS, tACS and tRNS Distributors List9.3 tDCS, tACS and tRNS Customers

10 Market Dynamics10.1 Market Trends10.2 Opportunities and Drivers10.3 Challenges10.4 Porters Five Forces Analysis

11 Production and Supply Forecast11.1 Global Forecasted Production of tDCS, tACS and tRNS (2021-2026)11.2 Global Forecasted Revenue of tDCS, tACS and tRNS (2021-2026)11.3 Global Forecasted Price of tDCS, tACS and tRNS (2021-2026)11.4 Global tDCS, tACS and tRNS Production Forecast by Regions (2021-2026)11.4.1 North America tDCS, tACS and tRNS Production, Revenue Forecast (2021-2026)11.4.2 Europe tDCS, tACS and tRNS Production, Revenue Forecast (2021-2026)11.4.3 China tDCS, tACS and tRNS Production, Revenue Forecast (2021-2026)11.4.4 Japan tDCS, tACS and tRNS Production, Revenue Forecast (2021-2026)

12 Consumption and Demand Forecast12.1 Global Forecasted and Consumption Demand Analysis of tDCS, tACS and tRNS12.2 North America Forecasted Consumption of tDCS, tACS and tRNS by Country12.3 Europe Market Forecasted Consumption of tDCS, tACS and tRNS by Country12.4 Asia Pacific Market Forecasted Consumption of tDCS, tACS and tRNS by Regions12.5 Latin America Forecasted Consumption of tDCS, tACS and tRNS13 Forecast by Type and by Application (2021-2026)13.1 Global Production, Revenue and Price Forecast by Type (2021-2026)13.1.1 Global Forecasted Production of tDCS, tACS and tRNS by Type (2021-2026)13.1.2 Global Forecasted Revenue of tDCS, tACS and tRNS by Type (2021-2026)13.1.2 Global Forecasted Price of tDCS, tACS and tRNS by Type (2021-2026)13.2 Global Forecasted Consumption of tDCS, tACS and tRNS by Application (2021-2026)14 Research Finding and Conclusion

15 Methodology and Data Source15.1 Methodology/Research Approach15.1.1 Research Programs/Design15.1.2 Market Size Estimation15.1.3 Market Breakdown and Data Triangulation15.2 Data Source15.2.1 Secondary Sources15.2.2 Primary Sources15.3 Author List15.4 Disclaimer

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QY Research established in 2007, focus on custom research, management consulting, IPO consulting, industry chain research, data base and seminar services. The company owned a large basic data base (such as National Bureau of statistics database, Customs import and export database, Industry Association Database etc), experts resources (included energy automotive chemical medical ICT consumer goods etc.

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tDCS, tACS and tRNS Market 2020 Outlook, Key Strategies, Manufacturers, Type and Application, Forecast To 2026 | Neuroelectrics, Magstim, NeuroCare...

Neuroscience

How a UCSF team is giving Cronutt the sea lion a second chance with neuroscience – University of California

A cellular therapy for epilepsy developed at UC San Francisco has been employed for the first time in a sea lion with intractable seizures caused by ingesting toxins from algal blooms. The procedure is the first-ever attempt to treat naturally occurring epilepsy in any animal using transplanted cells.

The 7-year-old male sea lion, named Cronutt, first beached in San Luis Obispo County in 2017 and was rescued byThe Marine Mammal Center(TMMC), based in Sausalito, Calif. His epilepsy is due to brain damage caused by exposure to domoic acid released bytoxic algal blooms. Each year, domoic acid poisoning affects hundreds of marine mammals, including both sea lions and sea otters, up and down the West Coast, a problem that is on the rise as climate change warms the worlds oceans, making algal blooms more common.

Like many of these animals, Cronutt cannot survive in the wild due to his epilepsy, and he was transferred by TMMC in 2018 to Six Flags Discovery Kingdom in Vallejo, Calif., which has facilities to care for wildlife with special veterinary needs.

In recent months, Cronutts health has declined due to increasingly frequent and severe seizures. With all other options exhausted, his veterinary team sought help from epilepsy researcherScott C. Baraban, Ph.D., in a last-ditch effort to save the sea lions life. For over a decade, Baraban, who holds the William K. Bowes Endowed Chair in Neuroscience Research in UCSFsDepartment of Neurological Surgery, has been developing the cell-based therapy, which has been shown by his research team to be highly effective in experimental lab animals.

This method is incredibly reliable in mice, but this is the first time it has been tried in a large mammal as a therapy, so well just have to wait and see, said Baraban, a member of the UCSF Weill Institute for Neurosciences. Over the years Ive come to learn how many marine mammals cant be released into the wild due to domoic acid poisoning, and its our hope is that if this procedure is successful it will open the door to helping many more animals.

On Tuesday, Oct. 6, a team of 18 specialists, including veterinarians from Six Flags and neurosurgeons and researchers from UCSF, successfully completed a precisely targeted injection of brain cell precursors taken from pig embryos called neural progenitor cells into Cronutts hippocampus, the brain region responsible for seizures. Based on extensive observations in rodents, Baraban said, the injected embryonic cells should migrate through his damaged hippocampus over the course of days and weeks, integrating and repairing the brain circuitry causing his seizures.

It was a remarkable convergence. Every year there are many animals suffering from epilepsy for which there isnt any treatment available, while, just across the bridge from The Marine Mammal Center, we at UCSF are trying to develop this new form of therapy and looking for ways to one day translate it to the clinic, saidMariana Casalia, Ph.D., a postdoctoral researcher who joined Barabans lab in 2015 to work ontranslating the groups successes in rodentsinto therapies, and who has taken the helm of the sea lion epilepsy project. It seemed very natural for us that these animals could be first patients to hopefully benefit from this therapy.

Domoic acid poisoning in marine mammals causes hippocampal damage very similar to that seen in temporal lobe epilepsy, the most common form of epilepsy in humans. In this disease, damage to hippocampal inhibitory interneurons removes the brakes on electrical activity, leading to seizures. In a vicious cycle, seizures can further damage brain circuitry, which is why epilepsy often worsens over time.

Since 2009, theBaraban labhas been developing a way to replace these damaged interneuronsby transplanting embryonic MGE (medial ganglionic eminence) progenitor cells into the hippocampus. As discovered two decades ago by Barabans UCSF colleaguesArturo lvarez-Buylla, Ph.D., andJohn Rubenstein, Ph.D., MGE cells normallymigrate into hippocampus during brain developmentandintegrate themselves into the local circuitry as inhibitory neurons.

Barabans group has shown that its possible to transplant embryonic MGE cells into the brains of adult rodents with temporal lobe epilepsy, wherethey quickly spread through the hippocampus and repair its damaged circuitry. The procedure reliably reduces seizures in these animals by 90 percent, along with other side effects of epilepsy, such as anxiety and memory problems.

Our laboratorys work has been inspired by the desire to find new solutions for the 30 percent of temporal lobe epilepsy patients who dont respond to available drug treatments, and for whom no new medicines have emerged over the past 50 years. Baraban said. For a number of reasons, including regulatory hurdles, cellular therapies for people with epilepsy are probably still a long way off. However, marine mammals with brain damage from domoic acid poisoning are in a very similar boat with no effective treatments that would let them ever be returned to the wild.

Baraban learned about the hundreds of annual domoic acidrelated strandings of marine mammals from long-time colleague Paul Buckmaster, D.V.M., Ph.D., of Stanford University. Buckmasters seminal studies in collaboration with TMMC in Sausalito had found that these animalssuffer from hippocampal damage almost identical to human temporal lobe epilepsy.

As soon as Mariana and I learned about this issue it was clear that our approach could be a perfect solution to help rehabilitate these animals, Baraban said.

Casalia had spent four years developing and testing a pig source of MGE cells pig tissue is often used for transplants into humans in collaboration with colleagues at UC Davis, work the lab intends to publish soon. On learning about the plight of domoic acidpoisoned sea lions, she partnered with TMMC and the California Academy of Sciences to study sea lion skulls to begin planning an eventual transplant surgery. She ultimately worked with UCSF neurosurgery chairEdward Chang, M.D., and collaborators at the medical software firmBrainLabto create a custom targeting system for the sea lion brain.She had even spent months working closely with the Hamilton Company to create a custom needle for delivering the stem cells to the right spot in a sea lions hippocampus.

All that remained was to find the right patient. And then, in September, 2020, they got a call from a veterinarian at Six Flags asking if they could help save the life of a sea lion named Cronutt.

After rescuing Cronutt in 2017, TMMC had attempted three times to rehabilitate him and release him back into the wild. Each time he would beach himself again, emaciated, disoriented, and approaching humans. Then he began to have seizures. Most marine centers dont have facilities for the long-term care of marine mammals with special needs, but Six Flags volunteered to give Cronutt a new home.

We have cared for a lot of special needs animals over the years, said Dianne Cameron, director of animal care at Six Flags. We adore Cronutt and are committed to providing him a forever home. He has his own apartment in our Sea Lion Stadium with a pool and dry resting area. When hes doing well, he comes out and participates in training sessions. Unfortunately, recently it has been hard to get him to come out of his apartment.

Over this spring and summer, Cronutt had begun a serious decline his seizures were increasing, he was losing weight, and he often seemed disoriented. To oversee Cronutts care, Six Flags hiredClaire Simeone, DVM, a founder and CEO of Sea Change Health, who hadstudied the neurological effects of domoic acid poisoningduring her six years working with TMMC. But it soon became clear that no treatment was working for Cronutt.

Despite our best efforts and all the tools that we have, his seizures were becoming more prolonged and more frequent over time, Simeone said. His brain damage and the effects on his body were getting worse. His decline has been gradual, but we reached a point several months ago where we were questioning what quality of life he had. We had run out of options for how we could successfully manage Cronutts disease and knew that we were going to have to make some hard decisions soon.

Then Simeone recalled a talk Baraban had given at TMMC several years ago about the potential of MGE transplants for marine mammals with domoic acid poisoning. In September, she reached out to ask if the lab might be willing to attempt the procedure as a last-ditch effort to save Cronutts life.

Cronutts health was slipping fast, but Casalias years of preparation for this moment allowed her and her colleagues to quickly assemble everything that would be needed in just one month.

In a bit of serendipity that would prove crucial, Cronutts brain had already been imaged in 2018 by Ben Inglis, Ph.D., of UC BerkeleysHenry H. Wheeler Jr. Brain Imaging Centeras part of an ongoing study ofhow domoic acid poisoning affects the sea lion brain. These MRI images provided critical guideposts that made it possible for UCSF neurosurgeons to plan how they would inject stem cells at just the right spot in Cronutts hippocampus.

Cronutts surgery, conducted in accordance with COVID-19 protocols at the SAGE Veterinary Centers in Redwood City, Calif., went smoothly, and he was returned to Six Flags. In the days after the surgery his veterinary team reported that he had been sleeping and eating well.

Based on prior experiments transplanting pig MGE cells into rats, the researchers expect it to take about a month or so for the cells to fully integrate into Cronutts hippocampus. They will be following up to see if his seizures decrease and his health and behavior improves, and whether his antiseizure medications can be reduced.

This first-ever attempt has been made possible by funding from a Javits Award from the National Institutes of Health and from the UCSFProgram in Breakthrough Biomedical Research. Without these funds, this kind of high-risk, high-reward science would never have gotten off the ground, Baraban added. It also depended on Marianas fearlessness and perseverance in pursuing this very uncertain project.

Casalia, who has degrees in applied science and neurobiology from Universidad National de Quilmes and the University of Buenos Aires in Argentina, says the surgery felt like a culmination of everything shed been working on in her career so far. Ive always wanted to apply what we are doing in the lab to the clinical setting, she said. For me the ability to do this in reality to help these animals who are suffering is a dream come true.

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How a UCSF team is giving Cronutt the sea lion a second chance with neuroscience - University of California