🧠 “The case for transmissible Alzheimer’s grows” (Scientific American). Genuinely a little frightening. Also consider this: neurosurgeons have a higher rate of Alzheimer’s than the general population.
The Case for Transmissible Alzheimer’s Grows
What separates a lethal prion from dementia-inducing amyloid plaque? Maybe not much
By Jennifer Frazer on February 7, 2019
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Alzheimer’s is not the only neurodegenerative disease in which aggregating misfolded host proteins – a class referred to as amyloid — seem to propagate and wreak havoc either. In Parkinson’s Disease, misfolded alpha-synuclein proteins spread through the brain, and in Amylotrophic Lateral Sclerosis (Lou Gehrig’s Disease), the misfolded, accumulating protein is TDP-43. We should investigate the transmission potential of these diseases as well.
The only thing that seemed to separate these conditions from classic prion diseases was transmissibility. But now that that barrier has been breached for at least one, I also wonder: What is the difference between amyloid and prions? Are they part of a spectrum? Are they one in the same? If not, what is the difference? Can what we’ve learned about the biology of prions help our efforts to fight amyloid dementias? Of course, since we still can’t cure prion diseases, it may not be much help even if so.
The realization that the peptides involved in some of the most common and feared dementias on Earth may be transmissible under even limited conditions is a sobering and humbling reminder of how very little we still understand about them. Given what we know about prions, I think we would be wise not to underestimate their abilities.
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This is really scary stuff to this old fart. It isn’t the Walking Dead where a bite turns you into a zombie, but a “sticky infectious prion” can wipe out your mind, life, and wallet. Hope a lot of someones are researching this. If I was a neurosurgeon, I be really concerned.
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