https://www.cbc.ca/radio/asithappens/as-it-happens-thursday-...
Tissue can be compressed, stretched, reorganized, or displaced especially to compensate for a congenital condition - the patient's brain had a lifetime to adapt to hydrocephalus, which pushed on the other brain tissue. The gray cortical shell is clearly visible in those images and their volume on a scan is not representative of neuron count or synaptic capacity.
There are far more dramatic cases of brain damage and neuroplasticity that reorganizes major functions, but there are a lot of caveats.
[1] https://www.thelancet.com/journals/lancet/article/PIIS0140-6...
That's why crows, with their low brain mass are pretty clever (and why all arguments equating brain size and smartness are wrong).
Just my layman understanding.
My understanding is that while brain cell death (outside of the hippocampus, at least) cannot regenerate, the connections and networks can.
But neurons regenerating connections between each other is, afaik, been pretty mainstream for awhile. The brain can't generate new cells, but it can rewire the connections between them, is what I understand. From reading the article, it seems to only claim rewiring connections, not regenerating cells.
There are a ton of upcoming drugs that help stimulating rewiring, for instance:
https://www.nia.nih.gov/news/new-drug-candidate-targeting-sy...
https://pmc.ncbi.nlm.nih.gov/articles/PMC8190578/
https://www.medicalnewstoday.com/articles/324410
etc.
But even though there are new brain cells growing, that does not mean you can reform lost structure.
An ischemic stroke (i.e. stroke due to a clot) caused by vascular or cardiac issues can be mitigated. A cryptogenic stroke however is idiopathic and therefore has no understood cause. These types of strokes make up 30-40% of all strokes. Unless we figure out their cause, there's no way to really prevent them.
But then there's also hemorrhagic strokes which are an entirely separate category that has causes and mitigations more or less diametrically opposed to those for ischemic strokes.
And of course those are just your broad painted categories and they are generally looked at as the start of a medical emergency but strokes happen all the time as a consequence of other medical emergencies.
Even if you could perfectly prevent strokes in generally healthy populations, those same people may still end up suffering from a stroke during a surgery or during/after a major accident or injury. No amount of preventative medication can prevent someone suffering a stroke caused by a brain bleed after a car accident. Likewise for someone with a crush injury, internal bleeding, or broken bones that end up throwing a clot which makes it into the brain.
So any advancement in halting and reversing damage from a stroke will be a massive boon for emergency medicine until the end of time. Unless of course we somehow find a way to cure/render humans immune to blunt force trauma or lacerations.
"DDL-920 is a potent, selective and brain permeable negative allosteric modulator (NAM) of the γ-aminobutyric acid type A receptors (GABARs), inhibits parvalbumin (PV) expressing interneurons (PV+INs) and consequently enhances γ-oscillations both in vitro and in vivo."
https://academic.oup.com/brain/article/148/6/1862/8052899?gu...
Sounds truly amazing, I have known two people who had severe strokes - one's PT was contingent on triaging resources to whoever was likely to recover more, another simply hated PT and speech therapy and often refused to participate or do the exercises. Even if it didn't help recovery a medicine like this would have reduced the stress of everyone involved.
>Carmichael and the team then identified two candidate drugs that might produce gamma oscillations after stroke. These drugs specifically work to excite parvalbumin neurons.
Asking while being total layperson here - can we generate those gamma oscillations by an [may be implanted] electronic device?
Edit: and google search to help, judging by the dates seems to be a pretty fresh field :
https://journals.plos.org/plosbiology/article?id=10.1371/jou...
"... by pairing robotic rehabilitation with a clinical-like noninvasive 40 Hz transcranial Alternating Current Stimulation, we achieved similar motor improvements mediated by the effective restoring of movement-related gamma band power, improvement of PV-IN maladaptive network dynamics, and increased PV-IN connections in premotor cortex. "
It also sounds like getting an exoskeleton for such patients can be helpful not only to perform immediate tasks, it also can be a part of the restoring process.
I think savvy universities want PIs who are savvy enough to realize that the point of these is to boost measurable visibility like citation count and h-index, so the headline of a news release boosting the article doesn't matter. They can always blame a copy editor for the headlines. It could read "world peace solved with moon juice." The provost would only care if it generated negative feedback. So it's the PR department's job to juice it as much as possible without getting blowback.
We can block certain arteries mechanically by inserting a tool, inject photosensitive agent then cause a targeted clot with a laser, inject clotting agent, choke, inject blood vessel dissolving agent and re-inject its own blood.
I understand why we research this but I just could not do it.
Also, the other definition in question is what the UCLA PR person means by "repairing brain damage". As far as I can tell from the paper - the "drug" part was using some neurotransmitter blockers on brain cells on a Petri dish to see if they could change gene expression or oscillatory firing patterns matching recordings in mice undergoing "physical therapy". They did not actually test to see if the stuff grew new brain cells or dendritic connections.
Does that mean it will neccesarily work? No, of course not. But its still exciting to see progress being made.
Mice are used only partly because they share a considerable amount of DNA with us. But they're mostly used because they're cheap. Both in financial and ethical costs.
They live for about two years, and breed in about three months. They are disposable. Over 100 million are killed each year in various labs across the country.
And for all of this, only about 5% of medicine that show positive animal results make it to market in some fashion. So basically, the best thing we can say about a mouse-tested drug is that "this most likely won't make things worse". But that's like a low bar.
In reality, if you have 100 5% chances of a cure for a previously incurable illness, you can celebrate each chance a lot.
These numbers are obviously entirely made up, but its worth noting that 100 5% chances of a cure, means you have at least 1 cure with (1-(.95)^100) = 99.4% probability.
If you are curing an incurable disease with 99.4% probability, celebrating a lot would be an understatement.
I'm surprised its that high tbh. And i suspect it would be a similar low number if we tested on humans instead of animals.
And yes, being able to test early stage ideas cheaply is critical to innovating. We use mice in biology for the same reason we use computer simulations in other fields.
Anyways, if we took your numbers of 5% chance at face value, that means there is a 1 in 20 chance of this press release turning into a real drug that saves real people's lives. Personally i dont think the chance is actually that high, but if it was that would only further my point that this is a milestone worth celebrating.
This is ignoring at least these benefits: surgery, development, genetic studies, grafts, anesthesia, and many MANY more. Some non-drug related, some drug adjacent, and they definitely have downstream benefits to humans.
Here's a survey paper with myriad examples: https://pmc.ncbi.nlm.nih.gov/articles/PMC9247923/
I really don't like when bioscience articles land here in HN because they are always commented on with:"in mice", as if to say nothing we see from mouse work works. Well, not everything is software and this kind of work takes years, if not decades. It is real science unfortunately which means that most of it doesn't work! Science, and bioscience specifically, are not efficient systems. In general, the things you do are hard and probably won't work. That doesn't mean you give up.
Animal models are not great, but they are the best progression we can do right now from cell models. And as for being disposable, there are controls on how animals are used in labs in the US: every institution that has animal experimentation has an IACUC (institutional animal care and use committee) that every research proposal must go through, and they do not a rubber stamp your proposal. They want to know why you can't use cell models, and why you can't do it with less or even no animals.
It would be nice if people were a bit more even handed when these types of articles come by. I think HN can do better.
An adage from the lab: "If what we did always worked it would be business, not science."
Let’s just skip straight to human trials.
I haven’t used psilocybin in a clinical setting but have gone through an alternative psychedelic-assisted therapy process. Very interesting results and many positives.
I've not tried that stuff since money is hard to come by these days. There have been a few human studies.
You can find more info here:
https://pubmed.ncbi.nlm.nih.gov/?term=bacopa+monnieri+cognit...
and here:
You perceive the idea as great not because you suddenly understand it better or know more. You think the idea is great because of the dopamine flooding your brain. And much like Dunning-Kruger, even thought you might think you did better, real world results don’t match your expectations.
