I would guess that the reason for this is mostly because Parksinson's itself is not that well understood.

It makes sense to say "yes it might work" because we know for sure the drug does xxxx and Parkinson's might have xxxx disease path and therefore cause xxxx which means xxxx symptom of Parkinson's might be due to xxxx which does respond to the drug

On the other hand it makes sense to say "no it might not work" because even though we know the drug does xxxx, Parkinson's might have alternative xxxx disease path and cause xxxx which means xxxx symptom of Parkinson's might be due to alternative xxxx which doesn't respond to the drug

I say it might work because either of these situations might be true

The top comment about it being too late for the actual cells is true, damage brain cells and connections can't be fixed but the damage can be prevented. I'm speaking on the prevention and/or slowing of disease progression

As other commenters mentioned, the word genetic did already exist

This quote essentially uses "genetic connection" in reference to what we now call "blood related"

But the thing that actually is crazy about Darwin in terms of genes is that he discovered natural selection, a phenomenon about genes, without knowing genes existed.

Evolution had be hypothesized / theorized for a long time before Darwin, it dates back to 495–35 BCE. Much of the terms he used in that book are not terms now, but were terms already developed by other evolutionary scientists prior to him using them. "genetic connection" had been used already to mean descended from the same being. The major evolutionist before Darwin was Lamarck, who coined and described many of the terms like that and described them quite accurately. Lamarck knew about inheritance and acquired traits already and did refer to this using terms like genetics, so Darwin did have that information.

Darwin did notice patterns that he assumed must be due to traits the animals must have in order for the patterns to be happening. He usually used the term "undergoing modification". He said many things that were about genes and inheritance without using modern terms before model, he definitely understood and noticed genetic patterns without figuring out what was causing them.

No, for example -people often hear a thudding type noise when they see something that looks like it is landing hard and causing vibration but not actually making noise

If you know about the concept of neuroplasticity -it has an effect on what noises we hear and causes what are kind of illusions. Native Hindi speakers can discern two different 'd' noises that sound the same to people who did not grow up hearing Hindi. English speakers can very easily discern the words "pen" and "pin" but many language speakers dissimilar to English cannot. German people who did not grow up hearing English (which today is essentially none of them) often could not perceive "th" sounds -if you've heard stereotypical German accents where "the" is pronounced like "ze", it is based on this -back in the day German people usually couldn't hear th sounds

If you've ever heard someone trying to learn a language or tried to learn a language yourself and just not been able to get certain sounds right -this is often why. When the brain did not grow connections to be able to perceive certain sounds, you cannot hear them and your brain creates an illusion of a sound you do know.

There are also tons of visual illusions that we perceive 24/7 the time but do not notice

It actually might. It is currently thought that they could slow or prevent some types of deterioration, but past studies failed due mainly to failure of the study methodology itself.

It seems intuitively right and I'm curious why it doesn't play out in reality.

here's essentially how it did play out in reality:

Researchers expected the drug to have a specific effect on the brain

Experimental studies were conducted. The hypothetical effect did in fact happen, and the brain did respond to the drug in a way that would delay disease progression.

Clinical studies on non-human primates were conducted, with the intent to see whether or not experimental findings translate to clinical study findings. The studies failed. The method in which the studies were conducted, especially in terms of the way researchers attempted to measure results, was not good and did not use very accurate measures that would reflect the potential impacts of the drug. There are many non-motor functions affected by Parkinson's that cannot be accurately measured in monkeys and apes(and were therefore not studied), like apathy, because they can't talk. These would have been the most important functions to study due to how the disease works.

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Current understanding is generally accepted as follows:

"Dopamine reuptake inhibition extends the stay of dopamine in the synaptic left. This pharmacologic principle may improve dopamine substitution in patients with Parkinson’s disease (PD). Experimental researchers described promising positive outcomes on the efficacy of inhibition of dopamine-, respectively monoamine reuptake (MRT). The translation of these findings into corresponding clinical study results for the treatment of patients with PD failed in the past. Further clinical development of MRT inhibition was suspended. One of several reasons was the missing clinical research focus on the effects of MRT inhibition on non-motor symptoms, like fatigue or apathy. Mandatory inhibition of glial inhibition of monoamine metabolism is a hypothetical but essential precondition for the efficacy of MRT inhibitors. Aforementioned reflections shall be considered, if the efficacy of the MRT inhibitor is again investigated in patients with PD. Resurgence of clinical research is warranted on the efficacy of MRT inhibition as a promising therapy approach for patients with PD."

This guy has written some articles about this, but doesn't really imply humans are able to survive there. He is an legit doctoral researcher, but not in anything relating about space. He just writes random articles for fun and isn't an actual authority figure on space.

A region of the layer of atmosphere 50-60km above the surface of Venus is thought to be the the most similar atmospheric conditions to Earth in our solar system. The atmospheric pressure and temperature of the air in this region is similar to ours, but the composition of gases is not exactly breathable.

So no, this layer would not be sustainable for human life.

As others have said, no it is not particularly unique in terms of the amount of species hosts it affects.

Animal cells come in different shapes and sizes but other than that, they are they are functionally and anatomically the exact same across different species. It does not matter much that we humans are closely related to other primates and not closely to birds, sea lions, etc. because we have the same cells either way.

The relevant part in terms of whether the virus can attach or not is due to things like different animo acid / receptors / acids covering the animal cell and preventing the virus from binding, host body temperature, the virus not producing enough of a particular protein to duplicate given the size/ immune system of their host, etc.

For example, rabies does not typically live in squirrels because their blood is not warm enough for the virus to be comfortable (~95 degrees F), but it does in raccoons (101-106 degrees F). The difference is not that significant but is enough to affect who the virus typically host.

Also,

>I know diseases like HIV are thought to come from primates, which makes sense: we're so closely related

Humans are primates :)

With modern understanding of pharmakinetics, researchers already have an idea of how drugs will act in mammals based on already understood compounds in or similar to the study drug. They can sometimes already tell what the half life is as well (this is how quickly the chemicals decay, or essentially stop working), so they know how long it will take for the drug to stop having an effect though it can behave differently in the body.

Study drugs are first administered to animals to determine potential AEs (adverse events, like side effects) and continue to study the half life by collecting blood and/or urine at specific intervals of time. Say they give the study drug at 8:00 am, they may draw blood or collect urine every 2 hours over the course of 12 hours. There will be less of the drug as time goes on, and they are using the blood/ urine samples to determine specifically how quickly it is passed though the body and how strong/ effective the medication is based on amount present in the sample.

Then they do the same thing in volunteer humans that get paid to be in a trial. They follow very strict procedures, the volunteers stay at the research facility 24/7 for a set period of time (could be a day could be 40 days) and are given the same food. The procedures (which includes when they administer the study drug or placebo, when they take blood or urine, when they take vital signs, EKG, weight, etc) are written out by the pharmaceutical company who developed the drug and are followed down to the second. Volunteers even need to pee at specified times. All adverse events (side effects) are recorded and there are usually follow up visits after the study volunteer is done with the initial stay to continue monitoring until the drug is no longer affecting them.

There are multiple arms of in-human studies where they do the same thing but with different diets, ethnicities, etc to see how the drug may be impacted by different factors.

So yes, they do a lot more than just blood testing and it is at very, very specific intervals of time. Usually vital signs, blood, urine, heart, etc are tested at specific times.

What you feel is situational dependent, and most areas of the body to not have the acuity for there to be a difference. What I mean by this is that the majority of the body is not sensitive enough for you to tell exactly where you are feeling something, and most nerves are so small that it is well below the threshold for being able to tell where the sensation is coming from exactly. There are also different types of mechanoreceptors that perceive touch, vibration, pressure, etc. differently and occur in different amounts over the body, so there is no one size all fits answer for perception related questions. In many cases you wouldn't feel anything, it would just be numb. The pain does physically "happen" in the pain receptors which are at the end of the nerves, though our sensation and perception is not fine tuned enough for us to feel a difference.

For example, if you put two pins next to each other on someones fingers with their eyes closed they would feel that there are two pins. The fingers have high acuity because of the type of mechanoreceptor + there are many small receptors and a large amount of brain dedicated to fingers. If you put two pins next to each other on someones back, they will feel as if there is only one. The nerve anatomy is not fine tuned enough on your back to be able to tell that there are two pins, and only one receptor is activated. Now imagine you put two microscopic pins a fraction of a millimeter away from each other. You wouldn't feel two different pins because the distance is so small, which is how nerves usually are. There are bigger nerves, like the ulnar nerve aka funny bone where you can feel more localized pain though it still is not that obvious where you are feeling the pain in terms of ending vs stem.