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I am very confident that finding the way the disease spreads from one cell to another is the key to stopping it. Below I have listed the hypotheses I have come across. The two first ones are "prion-like" spreading models where a misfolding of a protein causes further misfoldings in a self-repetitive manner (much like a neutron splitting a fissile nucleus causes more neutrons to emerge in nuclear reactors). The third one is also a self-propagating model driven by inflammation instead of the misfolded proteins, and the rest are models where an externally induced toxin drives the process in a non-self replicative manner.

The way I see it, any of them could be the correct one. However, the more I have studied, the more I am leaning towards the two top ones. And I am hoping it would be the one that goes through mitochondria, as that would offer more points of intervention.


infectious agent its target method of replication
misfolded protein mitochondria changing the ER conditions to cause further misfoldings
misfolded protein proteins being folded direct interference with the protein folding process
component of the immune system cell outer membrane causes Ca2+ influx and cell death, leading to further inflammation
BMAA protein assembly spreads diffusely, damaging new cells on its way
external toxin cell membrane spreads diffusely, damaging new cells on its way
borrelia spirochete cell membrane spreads diffusely, damaging new cells on its way