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A very interesting find: 

And, like all ALS related research should, open access to everybody! I am linking this picture in Chapter 2 for my own reference:

Figure 1. Multiple pathways of motor neuron degeneration and their therapeutic drugs in ALS: (1) increased Ca2+ in the motor neuron: dysfunction or downregulation of glutamate transporters such as GLT1 on the astrocytes, elevation of the Ca2+ permeable AMPA receptor via downregulation of or a deficit in the post-transcriptional edition of GluR2 sub-units, and mitochondrial dysfunction; (2) oxidative damage of the motor neuron: increased intracellular Ca2+ contents, high levels of mitochondria due to high energy demand, and increase in free metal ions such as copper and iron; (3) apoptosis in the motor neuron: activation of the Fas-mediated pathway, alteration of Bcl-2 family proteins via mitochondrial interaction with mSOD1, and initiation, propagation, or execution of caspase cascade; (4) inflammation: non-cell-autonomous motor neuron death (the disease progression is coordinated by mSOD1 expression in all neuronal and non-neuronal cells) and concurrent activation of the innate immune system and systemic inflammation (BBB breakdown may induce a vicious cycle of inflammation); and (5) autophagy: increased autophagosome formation. Current therapeutic drugs were developed basically against a specific route of ALS disease progression.