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The Case for Transmissible Alzheimer's Grows

blogs.scientificamerican.com

41–50 of 133 posts

Re: The Case for Transmissible Alzheimer's Grows

#41

Does this line of inquiry mesh at all with the idea that "Gum disease–causing bacteria could spur Alzheimer’s" Or are they competing hypotheses? reported here in January: https://news.ycombinator.com/item?id=18987015

I think some of it may be communication of "mental illness".

Re: The Case for Transmissible Alzheimer's Grows

#42
post #32

Earlier quoted context omitted.

Source?

https://thejns.org/abstract/journals/j-neurosurg/113/3/artic...

A possible explanation could be based on research suggesting that regular lack of deep sleep increases risk of Alzheimer’s. Given that Neurosurgeons have a grueling 7-8? year residency period after medical school, it would be possible that they undersleep far more than the control group.

I would like to see how the prevalence of Alzheimer's among Neurosurgeons compares against a population with similar work/sleep schedules (eg. finance)

Re: The Case for Transmissible Alzheimer's Grows

#43
post #27
post #25

Earlier quoted context omitted.

What eye exam(s) involve physical contact between the eyeball and a medical instrument? Or did a joke just go sailing over my head?

Checking eye pressure involves an instrument touching the eye, and is pretty routine.

Thank you, my eye tests have always used the air puff.

Re: The Case for Transmissible Alzheimer's Grows

#44

Dumb question (Wikipedia was of no help), if amyloid beta looks and acts like a prion, why isn't it classified as a prion?

Amyloid-Beta is a specific instance of amyloids, while prions are a class of amyloids:

>"Some amyloid proteins are infectious; these are called prions in which the infectious form can act as a template to convert other non-infectious proteins into infectious form." https://en.wikipedia.org/wiki/Amyloid

So if amyloid-beta is determined to be "infectious" (however that is done) then it would be put in the prion subclass of amyloids.

Re: The Case for Transmissible Alzheimer's Grows

#45

Does this line of inquiry mesh at all with the idea that "Gum disease–causing bacteria could spur Alzheimer’s" Or are they competing hypotheses? reported here in January: https://news.ycombinator.com/item?id=18987015

And related, does all of this mean that it is a good time for research into the causes of Alzheimer's because of lots of promising ideas, or a bad time, because there's no consensus?

Re: The Case for Transmissible Alzheimer's Grows

#46
post #42
post #32

Earlier quoted context omitted.

https://thejns.org/abstract/journals/j-neurosurg/113/3/artic...

A possible explanation could be based on research suggesting that regular lack of deep sleep increases risk of Alzheimer’s. Given that Neurosurgeons have a grueling 7-8? year residency period after medical school, it would be possible that they undersleep far more than the control group. I would like to see how the prevalence of Alzheimer's among Neurosurgeons compares against a population with similar work/sleep sch…

Do they ever stop? What does a surgeon do in their free time?

Re: The Case for Transmissible Alzheimer's Grows

#47
An increase in amyloids will be observed any time cells are malfunctioning for whatever reason.

They are the most thermodynamically stable structure that polypeptides can form, and require constant housekeeping to prevent. Accumulation of amyloids is like failing to taking out the trash in your house.

Afaik, there has never been a disease state checked for amyloids that failed to be associated with them (heart disease, cancer, stroke, etc).

>"From a wide range of in vitro experiments on peptides and proteins we now know that the formation of amyloid structures is not a rare phenomenon associated with a small number of diseases but rather that it reflects a well-defined structural form of the protein that is an alternative to the native state — a form that may in principle be adopted by many, if not all, polypeptide sequences

[...]

These observations, therefore, have led to the remarkable conclusion that, at the concentrations present in living systems, the native states may not always represent the absolute free energy minima of the corresponding polypeptide chains — the native form of a protein could in some cases simply be a metastable monomeric (or functionally oligomeric) state that is separated from its polymeric amyloid form by high kinetic barriers" http://www.ncbi.nlm.nih.gov/pubmed/24854788

I've previously commented the same thing:

https://news.ycombinator.com/item?id=14914528#14917057

https://hn.algolia.com/?query=amyloid%20nonbel&sort=byPopula...

Re: The Case for Transmissible Alzheimer's Grows

#48
post #9

The more we study the human body, the more questions we get. I wonder if some future Dr. McCoy centuries from now will we us as we do medicine of two centuries ago. We can go to other planets and invent new tech every day, but the body still holds a ton of mysteries.

Almost certainly. Medical professionals of the future will look at today’s cutting edge med tech the way we view blood-letting and balancing out the body’s humours.

Re: The Case for Transmissible Alzheimer's Grows

#49
post #46
post #42

Earlier quoted context omitted.

A possible explanation could be based on research suggesting that regular lack of deep sleep increases risk of Alzheimer’s. Given that Neurosurgeons have a grueling 7-8? year residency period after medical school, it would be possible that they undersleep far more than the control group. I would like to see how the prevalence of Alzheimer's among Neurosurgeons compares against a population with similar work/sleep sch…

Do they ever stop? What does a surgeon do in their free time?

From cursory googling it looks common for programs to expect you to work right up to the legal limit (80 hours/week based on 4-week averages) during residency. Having 16 hour days for ~7-8 years means that you probably have to get used to being a bit sleep deprived all the time.

Re: The Case for Transmissible Alzheimer's Grows

#50
I went to a talk recently [1] in which the researcher explained a theory of the origin of life where early cell membranes were based on amyloids. The theory can be described as ocean vent metabolism and amino-acid first (as opposed to tide pool and radiation/lightning RNA) and it's definitely not the most accepted theory but it's pretty interesting. Here's an open paper [2] and the speaker's homepage [3]

[1] https://www.eventbrite.com/e/ieee-buenaventura-embs-talk-fig...

[2] https://biologydirect.biomedcentral.com/articles/10.1186/174...

[3] https://science.jpl.nasa.gov/people/Russell/

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