It is worth noting that these topical applications are quite controversial in the medical literature. The evidence supporting a dermal absorption of magnesium (or other electrolytes) is pretty poor [1].
In theory, there is enough magnesium in your bones (~12 g) to cover your RDA (~400 mg) for 30 days [1]. However, only a third of that is available without strongly negatively affecting your health. So if your Mg stores are full (if!), then you have about 10 days worth "stored". However, your day-to-day Mg homeostasis is done by your kidneys, i.e. on a much, much shorter time scale. So your daily intake does matter, but sporadic deficiencies can be compensated for about 10 days.
> For example, let's say instead of gradient descent you want to do a Newton descent. Then maybe there's a better way to compute the needed weight updates besides backprop?
IIRC, feedback alignment [1] approximates Gauss-Newton minimization.
So there is an easier way, that is potentially biologically more plausible, though not necessarily a better way.
This is exactly the framing the author is criticizing. It assumes that the placebo effect is a constant that cannot be improved upon, and thus deserves no consideration, when designing the treatment. However, the placebo effect is malleable, and can be improved [1], In scientific studies, this is typically done through suggestions and conditioning [2]. However, this is not standard clinical practice (AFAIK).
Where the author is wrong, is that people that are designing drugs, aren't thinking about using the placebo effect more optimally. It is fairly well known, that the efficacy of drugs correlates with the severity of off-target side effects: say that you are taking an analgesic that acts by binding receptor A, but which also induces nausea by also binding an unrelated receptor B. During drug development, the structure of the drug is often tweaked to reduce or abolish binding to such off-target receptors, thus limiting side effects. However, these structural changes also often reduce efficacy, even if the affinity of the drug to the intended target isn't altered at all. My colleagues and I (working in pharmacology but in academia) have often wondered to what degree drug companies try to actively keep non-severe side effects as part of the response profile, given that they may be beneficial for the treatment outcome.
There are dozens of us! Mostly because Nedergaard's lab(s) are like 50 people all by themselves.
I always find it interesting what people's perception of the size of academic subfields is. For most topics in the biological sciences (i.e. excluding cancer, HIV, malaria, AD, and other "whales") you can fit everyone that has directly worked on that topic in the last 5 years in a medium-sized auditorium. And many people work on multiple topics!
I am also not a fan of the pivot to Snap. However, it is worth mentioning, that it has only been two years (I think, at least 22.04 LTS was the first release I had to wrestle with them on my machine), and the experience has become a lot better during this time.
You are referring to the critical period [1] of (second) language acquisition, which is generally thought to end with the onset of puberty [2].
Neurodevelopmentally, this period coincides with extensive synaptic and dendritic pruning and increased myelination (of axons) [3], which result in the loss of some connections and the strengthening and acceleration of others. Cell loss is not thought to be a major driver of brain maturation, nor is it thought to occur more frequently during this time window.
> I find I feel more rested with more REM cycles which generally means REM starts earlier.
This is probably the case because your NREM / slow-wave sleep need was low to begin with. If you go to bed relatively rested, it's easy to be fully rested when you wake up. REM is typically delayed when you are exhausted.
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC5579607/