[esm]

Spores formed by bacteria like C. botulinum or B. anthracis are also very difficult to neutralize. The key is knowing if there is an exposure risk and taking added precautions.

The good news is that some people are "immune" to developing an infectious prion disease. Turns out that certain mutations prevent normal proteins from interacting with a complementary prion in a way that would cause them to become misfolded.

[djsumdog]

So for people with Alzheimer's disease, is that plaque always associated with prions/protein mis-folding? (and if so, is it worthless to do things like "Learn a second language," "Learn to play more instruments," etc because our brain usage doesn't really play into the development of Alzheimer's? It's mostly a genetic thing?

[esm]

It's an unsatisfying answer, but Alzheimer's (and most disease for that matter) is a combination of genetic risk and what you do with your life. It is hard to know exactly how much genes or the environment contribute. There are subsets of neurodegenerative diseases that are almost entirely genetic (Huntington's, some forms of Parkinson's, etc.) and some that are almost 100% environmental (there's an interesting story about a group of IV drug users in San Francisco who developed Parkinson's after taking something laced with MPTP). Most cases are somewhere in the middle though.

Learning other languages or instruments is probably useful from a brain health standpoint regardless of your genetics (even if you already have early-stage AD you can slow progression), but they are just proxies for activity. I would guess that learning something that interests you is more important than what that thing actually is.

[rbanffy]

I guess it's more complicated than that. Brain usage affects its chemistry - how much of what is available where - which, in turn, may have an effect on how misfolded proteins interact with normal ones.

Keep in mind I'm no expert, but this seems to be a reasonable assumption.