Neuroscience: News and Discussions.
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What was the most impactful Neuroscience article, discovery, or content of the year? (self.neuroscience)
submitted 7m ago by NickHalper
What makes it so impactful? What was special about it?
Alternative_Belt_389 86 points 7m ago
The litany of high-impact journals that published several very positive studies regarding psychedelics and mental health.
BigFaceCoffeeShop 43 points 7m ago
It's almost like we were ready, scientifically, for this in the 70s, then *something* got in the way.
Wonder where psychopharmacology would be today if the Harvard Psilocybin Project was never shut down.
Wonder where psychopharmacology would be today if the Harvard Psilocybin Project was never shut down.
Alternative_Belt_389 5 points 7m ago
God right?? People act like all if this is new when really it's been a part of so many Iives for thousands of years; no respect either for indigenous use. I'm outraged more so for cannabis research since it is an incredible plant that can help a much wider range of conditions.
Brain_Hawk 16 points 7m ago
I agree this is exciting stuff. But there is a dark side.
The same data is being recycled over and over again.and there are more reviews than primary research article. Sign of a hot topic kn mass hype train that Needs more actual research.
Optimistic, and excited to be involved in this growing field, but it's important we don't inflate the value of these drugs. They will not be miracle cures, despite the hype. Maybe another important alternative to the psychiatric toolbox, maybe really effective for some. But little data suggesting sustained (e.g. 6 months) effects.
I'm excited, but also cautious. Much more work needed
The same data is being recycled over and over again.and there are more reviews than primary research article. Sign of a hot topic kn mass hype train that Needs more actual research.
Optimistic, and excited to be involved in this growing field, but it's important we don't inflate the value of these drugs. They will not be miracle cures, despite the hype. Maybe another important alternative to the psychiatric toolbox, maybe really effective for some. But little data suggesting sustained (e.g. 6 months) effects.
I'm excited, but also cautious. Much more work needed
Alternative_Belt_389 7 points 7m ago
I am extremely cautious as well mostly because of the ethical concerns of treatment. Many therapists have sexually abused patients while taking psychedelics and that is underecognized. In addition clinicians need to understand the very important role that set and setting play in the healing experience.
Brain_Hawk 12 points 7m ago
I've never heard of this, very concerning if it's really a prevalent problem.
The darkest side is how many for profit companies are jumping on this. It's gonna be the wild west. And a lot of them are gonna care a lot less about providing care than making a profit. And yes, opens opportunities for exploitation.
The darkest side is how many for profit companies are jumping on this. It's gonna be the wild west. And a lot of them are gonna care a lot less about providing care than making a profit. And yes, opens opportunities for exploitation.
Alternative_Belt_389 4 points 7m ago
Absolutely! It may really help patients but we need a very strict medical model to do so.
East-Ad8159 3 points 6m ago
Valid statement! Overvaluation of these drugs with the same data that recycled could cast a cloud on the actual benefits.
Burbly2 3 points 7m ago
Could you link to some of the papers, please?
Alternative_Belt_389 2 points 7m ago
There are so many! I would do a search for mental health and psilocybin to start
NeuroscienceNerd 2 points 7m ago
Yes this!!
FoundinNewEngland 1 points 7m ago
There’s one I’d like to discuss with you specifically
Alternative_Belt_389 1 points 7m ago
Feel free to message me!
atritt94 1 points 2m ago
It is very beneficial.
avajiyo 1 points 6d ago
Is there any particular substance nominated? Think I've watched a couple of Netflix documentaries that shifted my perspective on psychedelics to a bit more positive side, but I'd still be too scared to try having experienced a severe panic attack from Marijuana consumption.
Alternative_Belt_389 2 points 6d ago
Cannabis and psychedelics are very different and each have their own mechanism of action. Once psilocybin is legalized, I would recommend going the clinical route and doing a guided session with a therapist. Psychedelics are very safe but always come with a risk of potential adverse effects
avajiyo 2 points 6d ago
Thanks. I'll note that.
Alternative_Belt_389 2 points 5d ago
I'm not a clinician but based on what I know!
BorneFree 82 points 7m ago
In my opinion, it’s pretty easily the finding that EBV associates with MS to a high degree of confidence (link)
The impact, the size and validity of the study, the implications in future MS research are all extremely impressive
The impact, the size and validity of the study, the implications in future MS research are all extremely impressive
Dirzicis 21 points 7m ago
For those that don't know (in case you are just interested in neuroscience and are not a researcher yourself). The Epstein-Barr Virus (EBV) is the virus that causes infectious mononucleosis (Mono). One study thinks this disease is linked in some way to Multiple Sclerosis. MS is a serious neurological disease that can cause you to be bedbound and lose coordination and control of your muscles among other things.
If true, his has huge implications for everyone because mononucleosis is extremely easy to transmit. So much so, that it is referred to as "the kissing disease". However, it still needs to be replicated by other studies.
If true, his has huge implications for everyone because mononucleosis is extremely easy to transmit. So much so, that it is referred to as "the kissing disease". However, it still needs to be replicated by other studies.
Leading_Pickle1083 2 points 5m ago
This study is suggestive of a causal relationship?
atritt94 1 points 2m ago
That’s wild
phatspatt 15 points 7m ago
"This conclusion would be robust even in the very unlikely case that EBV seroconversion in one of the MS cases was a false-positive result, in which case EBV infection would confer a 16-fold increase in MS risk."
it amazes me how you start with millions, and then the strength of association, or whether one exists, rests with just a couple of assay wells looking for a bit of a darker color in seroconversion.
i hope it can be replicated, but history has not been kind to these types of observations
it amazes me how you start with millions, and then the strength of association, or whether one exists, rests with just a couple of assay wells looking for a bit of a darker color in seroconversion.
i hope it can be replicated, but history has not been kind to these types of observations
Exciting_Feeling_657 9 points 7m ago
https://open.spotify.com/episode/4qvFh5tpjwrTQ4vPDOsxZe?si=e522785847d04887
Podcast episode covering this! Interesting interview with the lead scientist
Podcast episode covering this! Interesting interview with the lead scientist
SelfAwareMachine 9 points 7m ago
Have you seen any replication studies with similar/same results? I've been keeping an eye on this but I haven't seen a whole lot develop from it.
MS is still largely a clinical disease, and results which map so completely with clinical diseases (and all their built in subjective diagnostic requirements), IMO, should be treated suspiciously. It feels like finding a condition (outside of SES) with causality to psychiatric conditions, when the diagnostic reliability (particularly inter-rater) of clinical conditions is pretty mediocre (generously). I'm still not certain that these results weren't the product of the ubiquity of EBV.
A replication would be massively improved by including pediatric MS patients and including results which diversify the environmental factors more. Limiting the scope to adults in the military or adjacent to military members/bases excludes too many populations where MS exists and EBV infections do not.
Also, this article: Scientists Debate the Role of a Virus in Multiple Sclerosis is a pretty insightful look at other reactions to the work.
MS is still largely a clinical disease, and results which map so completely with clinical diseases (and all their built in subjective diagnostic requirements), IMO, should be treated suspiciously. It feels like finding a condition (outside of SES) with causality to psychiatric conditions, when the diagnostic reliability (particularly inter-rater) of clinical conditions is pretty mediocre (generously). I'm still not certain that these results weren't the product of the ubiquity of EBV.
A replication would be massively improved by including pediatric MS patients and including results which diversify the environmental factors more. Limiting the scope to adults in the military or adjacent to military members/bases excludes too many populations where MS exists and EBV infections do not.
Also, this article: Scientists Debate the Role of a Virus in Multiple Sclerosis is a pretty insightful look at other reactions to the work.
CHneurobio03 2 points 7m ago
>(link)
SelfAwareMachine 59 points 7m ago
I think this was actually released December 2021, but it's probably the neuroscience article I've cited more than any other this year: From Synapses to Circuits, Astrocytes Regulate Behavior. I think this set the stage for the flood of glia focused work in 2022, and that's resulted in a pretty tremendous amount of insight across the board.
Sanger put out a few pieces of work which greatly expanded our interactome maps, which was also pretty amazing, summary here: First map of immune system connections reveals new therapeutic opportunities. While less obviously "neuroscience" for behaviorists, the underlying protein mechanics govern cellular interactions in a very broad way throughout the nervous system, and these interaction maps provide a pretty strong step toward a better understanding of the metabolic complexity we previously didn't really grasp.
As a whole, the work which is establishing glia as the metabolic substrate of the nervous system feels like it has the capacity to improve our understanding of function in a paradigm shifting way.
Sanger put out a few pieces of work which greatly expanded our interactome maps, which was also pretty amazing, summary here: First map of immune system connections reveals new therapeutic opportunities. While less obviously "neuroscience" for behaviorists, the underlying protein mechanics govern cellular interactions in a very broad way throughout the nervous system, and these interaction maps provide a pretty strong step toward a better understanding of the metabolic complexity we previously didn't really grasp.
As a whole, the work which is establishing glia as the metabolic substrate of the nervous system feels like it has the capacity to improve our understanding of function in a paradigm shifting way.
3L1T 11 points 7m ago
Thanks for this post.
bertyl 67 points 7m ago
In my opinion it was de meta review showing that depression is not caused by a chemical imbalance in the brain (link). For decades the thinking was that depression was the result of too little serotonin, a hypothesis that was constructed after the observation that antidepressants (SSRIs) work by elevating the availability of serotonin. Now it's becoming clear that antidepressants don't work as well as previously thought, or even not at all (compared to placebo). These insights will be very impactful in our thinking about depression and how we help people who suffer from it.
Kawa-iMilliye 15 points 7m ago
Yeah, don't think they are completely useless but was one of the best findings recently
Brain_Hawk 12 points 7m ago
There are significant number of concerns in caveats with the very simple explanation you've provided of this paper, which is how many people have replied to it. There is Decades of evidence that antidepressants and serotonergic medications are effective in a good proportion of the population. Nothing about this paper or This research demonstrates that's not the case.
What's more, just because these guys didn't find evidence of serotonergic relationships doesn't mean they're not there. There's pretty high quality evidence from early studies using pet of serotonergic effects and depression. But like all mental health, depression is complicated, and this single cause was never going to be the answer. People describing it as a chemical imbalance already represents a wildly simplistic View of how mental health and the brain works
The last point I want to raise is just because serotonin isn't the necessary cause of all depression, doesn't that classic saratogenergic drugs won't work. Just because depression may not be caused by a lack of Serotonin doesn't mean that improving serotonin won't improve depression. A good example of somebody used for this, is that headaches are not caused by the lack of acetaminophen. But acetaminophen still helps headaches
There were some important points racing that paper, but it's been taken a lot of context and excessively simplistically, including I think by the authors themselves.
And honestly, I think this is one of those papers that may do more harm than good. Because people are going to start saying depression doesn't involve serotonin, so I shouldn't take medication. Some people are a lot better off medicated. For some people, ultimate theories are probably better, but ssris have been life-changing for some people
What's more, just because these guys didn't find evidence of serotonergic relationships doesn't mean they're not there. There's pretty high quality evidence from early studies using pet of serotonergic effects and depression. But like all mental health, depression is complicated, and this single cause was never going to be the answer. People describing it as a chemical imbalance already represents a wildly simplistic View of how mental health and the brain works
The last point I want to raise is just because serotonin isn't the necessary cause of all depression, doesn't that classic saratogenergic drugs won't work. Just because depression may not be caused by a lack of Serotonin doesn't mean that improving serotonin won't improve depression. A good example of somebody used for this, is that headaches are not caused by the lack of acetaminophen. But acetaminophen still helps headaches
There were some important points racing that paper, but it's been taken a lot of context and excessively simplistically, including I think by the authors themselves.
And honestly, I think this is one of those papers that may do more harm than good. Because people are going to start saying depression doesn't involve serotonin, so I shouldn't take medication. Some people are a lot better off medicated. For some people, ultimate theories are probably better, but ssris have been life-changing for some people
[deleted] 3 points 6m ago
The "life-changing" positive effect of antidepressants has been proven to be due to placebo effect https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4172306/. And the side-effects, often irreversible, have sadly been drastically underplayed for decades.
Brain_Hawk 10 points 6m ago
That's a single Paper by a single author published in a not particular prestigious journal, that has been very thoroughly called into question by many people.
Placebo effects are very real, we are well aware of their power. But there is a large body of research indicating a positive effective antidepressants.
I have certainly seen no evidence that the side effects were permanent. Everything I'm aware of is that side effects tend to stop when the medication stops, which is the case for the majority of drugs in general
Placebo effects are very real, we are well aware of their power. But there is a large body of research indicating a positive effective antidepressants.
I have certainly seen no evidence that the side effects were permanent. Everything I'm aware of is that side effects tend to stop when the medication stops, which is the case for the majority of drugs in general
[deleted] 7 points 6m ago
You are right that there unfortunately has not yet been more extensive research regarding the topic. I'm surprised though that you haven't heard about the permanent side effects, I thought this fact was more widely known. It happened to me and several other people I know, although I'm of course still hoping my SSRI-induced health issues are not permanent and will go away one day after all... I've heard very similar stories from many other people who got permanent health problems after taking antidepressants. You might be interested in reading these articles https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6839490/, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8061256/, and checking people's stories on r/antipsychiatry.
Regarding the purported positive effect of antidepressants... SSRIs are given to people under the explanation that the problem is chemical imbalance in their brain, yet no one measures or monitors a patient's serotonin levels when prescribing them an SSRI, and what's more, the doses are prescribed basically at random. I was treated by two prestigious psychiatrists with PhDs and they would tell me to increase the dose when I expressed my concerns that the pills weren't helping...can you imagine, for example, a diabetes patient whose insulin levels are not measured or monitored and insulin is given at random instead? No, because there is actual evidence and mechanism to the treatment of diabetic patients, while with depressed patients it's just "we don't measure your serotonin levels, but just trust us, your problem is that you need more serotonin, so here are some pills for that".
I'm sorry if my reply is rather lengthy, it's just that I've had a lot of experience with different SSRIs/SNRIs and they badly screwed up several years of my life, and I'm tired of the lies still perpetuated about them, especially after meeting several other people with similar stories and experiences. Again, if you're open to it, I would recommend checking the antidepressant stories on r/antipsychiatry; even if you disagree that SSRIs are very harmful, I think it's important to be at least aware of what many people's experiences with them have been.
Regarding the purported positive effect of antidepressants... SSRIs are given to people under the explanation that the problem is chemical imbalance in their brain, yet no one measures or monitors a patient's serotonin levels when prescribing them an SSRI, and what's more, the doses are prescribed basically at random. I was treated by two prestigious psychiatrists with PhDs and they would tell me to increase the dose when I expressed my concerns that the pills weren't helping...can you imagine, for example, a diabetes patient whose insulin levels are not measured or monitored and insulin is given at random instead? No, because there is actual evidence and mechanism to the treatment of diabetic patients, while with depressed patients it's just "we don't measure your serotonin levels, but just trust us, your problem is that you need more serotonin, so here are some pills for that".
I'm sorry if my reply is rather lengthy, it's just that I've had a lot of experience with different SSRIs/SNRIs and they badly screwed up several years of my life, and I'm tired of the lies still perpetuated about them, especially after meeting several other people with similar stories and experiences. Again, if you're open to it, I would recommend checking the antidepressant stories on r/antipsychiatry; even if you disagree that SSRIs are very harmful, I think it's important to be at least aware of what many people's experiences with them have been.
Psychdoctx 1 points 2m ago
Don’t SSRI’s have anti inflammatory effects which could help decrease inflammation caused by infectious diseases. Many of my depressed patients had diagnosis of auto immune diseases.
juicymooseMA 5 points 7m ago
Thanks for providing this, this is extremely interesting and I wouldn’t have found this if you didn’t post this
Cultivate88 2 points 6m ago
From someone without any neuroscience background, I had always thought that depression was a lack of dopamine (lack of motivation).
atritt94 1 points 2m ago
This is a good article- touches on the complexity of this and how it is not ^ that simplistic actually.
https://www.tandfonline.com/doi/full/10.31887/DCNS.2002.4.1/bbondy
“Although repeated data showing decreased levels of the NE metabolite a-methoxy-4-hydroxyphenylglycol (MHPG), which indicates NE. turnover in brain, support the hypothesis of a deficient noradrenergic system,Citation38 the results are inconsistent.Citation39 Similarly to the noradrenergic system, the data on determinations of 5-HT and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) could not prove the hypothesis of exclusively reduced serotonergic transmission. Many studies reported decreased central serotonergic turnover in major depression; but findings also suggested that reduced 5-HT function may not be present in all depressed patients.Citation42 These discrepancies between studies may reflect both methodological problems, such as difficulties in measuring the amines after various postmortem delays, and the fact that determinations of neurotransmitters or their metabolites in CSF or blood reflect a summation of many events in many brain areas and not in restricted nuclei.”
https://www.tandfonline.com/doi/full/10.31887/DCNS.2002.4.1/bbondy
“Although repeated data showing decreased levels of the NE metabolite a-methoxy-4-hydroxyphenylglycol (MHPG), which indicates NE. turnover in brain, support the hypothesis of a deficient noradrenergic system,Citation38 the results are inconsistent.Citation39 Similarly to the noradrenergic system, the data on determinations of 5-HT and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) could not prove the hypothesis of exclusively reduced serotonergic transmission. Many studies reported decreased central serotonergic turnover in major depression; but findings also suggested that reduced 5-HT function may not be present in all depressed patients.Citation42 These discrepancies between studies may reflect both methodological problems, such as difficulties in measuring the amines after various postmortem delays, and the fact that determinations of neurotransmitters or their metabolites in CSF or blood reflect a summation of many events in many brain areas and not in restricted nuclei.”
[deleted] 1 points 4d ago
Worth pointing out, there has been a ton of methodological pushbacks to the Moncrieff rv, from many angles
https://www.nature.com/articles/s41380-023-02095-y
https://www.kcl.ac.uk/news/a-response-to-the-serotonin-theory-of-depression-a-systematic-umbrella-review-of-the-evidence
I’m not fully settled on where I stand on the issue (my doctoral work was on large scale brain networks of AD, I got no where near depression), but it is certainly not an open and shut case
https://www.nature.com/articles/s41380-023-02095-y
https://www.kcl.ac.uk/news/a-response-to-the-serotonin-theory-of-depression-a-systematic-umbrella-review-of-the-evidence
I’m not fully settled on where I stand on the issue (my doctoral work was on large scale brain networks of AD, I got no where near depression), but it is certainly not an open and shut case
ChickenAndRiceIsNice 21 points 7m ago
Not so much an article but an idea... Geoff Hinton gave a keynote address during NeurIPS 2022 (a couple of weeks ago) about how the advancement of artificial intelligence lies in forward-forward processing. The difference between that and the usual back propagation technique is that another, separate process is used to improve learning in another forward process. This means the computational load on learning can be done in real time, rather than the computationally expensive task of back propagation. Some of these points were also highlighted by Jürgen Schmidhuber in his keynote during the same conference.
How does this relate to neuroscience? Well, Geoff mentioned that a possible reason for why we sleep is to perform a similar forward-forward processing task in our brains to improve learning from the barrage of data we absorbed while awake. The reason why such a hypothesis is remarkable is because we are starting to uncover things about our own brains by optimising artificial intelligence, which we largely created with inspiration from our own brains. I haven't summarised the talk very well here because it would need quite a lot more space for explanation, but I'm sure one will be provided by others better at describing these things than I can in the close future.
How does this relate to neuroscience? Well, Geoff mentioned that a possible reason for why we sleep is to perform a similar forward-forward processing task in our brains to improve learning from the barrage of data we absorbed while awake. The reason why such a hypothesis is remarkable is because we are starting to uncover things about our own brains by optimising artificial intelligence, which we largely created with inspiration from our own brains. I haven't summarised the talk very well here because it would need quite a lot more space for explanation, but I'm sure one will be provided by others better at describing these things than I can in the close future.
SelfAwareMachine 8 points 7m ago
Experience-dependent structural plasticity in the adult brain: How the learning brain grows - Do we sleep to allow astrocytes a metabolic break time to transcribe "learned" information to their local environments?
Learning-related contraction of gray matter in rodent sensorimotor cortex is associated with adaptive myelination - What that transcription process looks like?
Edit: IMO the primary flaw of CompNeuro is imagining nervous systems, or brains in particular, are optimized for anything other than maintaining a metabolic niche. Processing/computing is an artifact of metabolic function rather than a driver of it.
Learning-related contraction of gray matter in rodent sensorimotor cortex is associated with adaptive myelination - What that transcription process looks like?
Edit: IMO the primary flaw of CompNeuro is imagining nervous systems, or brains in particular, are optimized for anything other than maintaining a metabolic niche. Processing/computing is an artifact of metabolic function rather than a driver of it.
saltyPeppers47 4 points 7m ago
What I didn’t like was this: “The algorithm scales much better than reinforcement learning and would be much easier to implement in cortex than backpropagation.” Assuming he’s talking about a biological cortex (and not some NN), it seems to ignore the fact that backpropagation is a well-established physiological phenomena. A general critique of the comp neuro field that I have had is how some folks just ignore biological evidence altogether and then make claims about how the brain could work.
monkeysingmonkeynew 2 points 6m ago
Sounds interesting, any links to posters/articles on the topic?
bushy5000 29 points 7m ago
I think it has to be the success of Lecanemab in reducing amyloid in the brain and slowing cognitive decline! Obviously there’s still so much further to go in treating Alzheimer’s, not only with amyloid but other pathological markers like tau, inflammation etc, but this feels like an amazing shift in a disease where up until now no real “cure” has existed.
phatspatt 8 points 7m ago
well, several other drugs in recent years, bace inhibitors, adecan, etc, cleared amyloid. perhaps this one lies with the protofilament targeting, versus the fixation on oligomers in the past.
u get my upvote!
u get my upvote!
BorneFree 4 points 7m ago
Oof be prepared for downvotes from the anti amyloid people
Little4nt 5 points 7m ago
In the words of Francisco Gonzalez Lima, amyloid is unrelated to pathology
martland28 1 points 6m ago
> up until now no real “cure” has existed
And still doesn’t…? What do you mean by cure.
And still doesn’t…? What do you mean by cure.
bushy5000 1 points 6m ago
Quote marks suggested not an actual cure - more so implying something that directly targeted pathology rather than just patching up symptoms, but definitely the first step towards an actual cure
martland28 1 points 6m ago
Good thing there are other studies that have had success treating pathology and symptoms. But I think it’s too soon to say which of these is a step towards a definitive cure.
lambda_mind 38 points 7m ago
For me personally, Cortical Labs teaching neurons to play Pong. I like the Free Energy principle anyway, and seeing it applied like this is super cool.
[Link](https://www.cell.com/neuron/fulltext/S0896-6273(22\)00806-6?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0896627322008066%3Fshowall%3Dtrue)
[Link](https://www.cell.com/neuron/fulltext/S0896-6273(22\)00806-6?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0896627322008066%3Fshowall%3Dtrue)
colacolette 5 points 7m ago
This is CRAZY. Something I had never even really considered could be possible.
Orangutansin 3 points 6m ago
In the field of neuroprosthetics a lot of research has been done on directly stimulating retinal ganglion cells it’s electrodes, but it hasn’t been super effective because electrodes would stimulate all nearby rgcs but scientists have figured out a way to selectively stimulate specific Rrtinal ganglion cells as the EPSPs matched those of normal physiological retinal ganglion cells
https://iopscience.iop.org/article/10.1088/1741-2552/ac861f
https://iopscience.iop.org/article/10.1088/1741-2552/ac861f
longdongdisease 3 points 2m ago
Can't believe no one has posted the publishing of the larval *Drosophila* connectome with over 3000 neurons by Winding et al 2023
https://www.science.org/doi/10.1126/science.add9330
https://www.science.org/doi/10.1126/science.add9330
FromTheLabBench 2 points 2m ago
The deadline (May 1) is approaching for applying for this PAID fellowship opportunity to earn a Master's in data science and work with real-world dementia data at the NIH Center for Alzheimer's and related dementias! It's seriously such a unique opportunity.
Please share this with any students you know interested in #datascience, #neuroscience or #aging!
Learn more: https://card.nih.gov/job-training-opportunities/training-opportunities/data-science-masters
Please share this with any students you know interested in #datascience, #neuroscience or #aging!
Learn more: https://card.nih.gov/job-training-opportunities/training-opportunities/data-science-masters
Due_Cartographer9453 2 points 2m ago
This discussion...The idea of the neuroscience of the future self is that our brain creates a connection between our current self and our desired or future self. Neuroscientists believe that the brain treats our future self in a similar way to how it treats other people. This connection between our current self and our future self can help us to make better decisions in the present. Join our founder Linda Ray along with the team, on her mission of changing the world one brain at a time.
https://neurocapability.com.au/about/
https://neurocapability.com.au/about/
RealJakeyPooV 1 points 3m ago
Tubulars, fr fr
atritt94 1 points 2m ago
https://news.yale.edu/2021/07/05/psychedelic-spurs-growth-neural-connections-lost-depression
“In a new study, Yale researchers show that a single dose of psilocybin given to mice prompted an immediate and long-lasting increase in connections between neurons. “
“In a new study, Yale researchers show that a single dose of psilocybin given to mice prompted an immediate and long-lasting increase in connections between neurons. “
Unlikely_Scapegoat 1 points 8d ago
I am most intrigued by Interoception. We seem to get be getting closer to understanding intuition and a different degree of consciousness.
avajiyo 1 points 6d ago
Organoid intelligence (OI): the new frontier in biocomputing and intelligence-in-a-dish
https://www.frontiersin.org/journals/science/articles/10.3389/fsci.2023.1017235/full
Talks from ppl like Andrew D. Huberman, Dr.K (HealthyGamerGG), and Kelly McGonigal were also very insightful.
https://www.frontiersin.org/journals/science/articles/10.3389/fsci.2023.1017235/full
Talks from ppl like Andrew D. Huberman, Dr.K (HealthyGamerGG), and Kelly McGonigal were also very insightful.
[deleted] 1 points 4d ago
On one hand, I want to say the ENGAGE, EMERGE, and CLARITY trial papers…but that’s the clinical neuro bias in me
True neuroscience wise it’s Braakspear’s “Geometric constraints on human brain function” or the Marek paper on sample size required in BWAS findings
We’ve learned a lot this past year in terms of best practices and ways forward for the field of functional MRI, especially for rs
The question that remains, at least for my field of expertise (AD and related dementias) is how big of a role fMRI will continue to take with biomarkers changing as they are
True neuroscience wise it’s Braakspear’s “Geometric constraints on human brain function” or the Marek paper on sample size required in BWAS findings
We’ve learned a lot this past year in terms of best practices and ways forward for the field of functional MRI, especially for rs
The question that remains, at least for my field of expertise (AD and related dementias) is how big of a role fMRI will continue to take with biomarkers changing as they are
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