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Posted On: 02/21/2021 6:00:52 PM
Post# of 145871
Certainly an interesting thread there as to the exact mechanism of ALS causation in SOD1 ALS.
This 2001 article says mutant SOD1 is not sufficient for ALS in some special mice.
https://www.jneurosci.org/content/21/10/3369.short
Then in 2008 this article with exactly the opposite claim, that SOD1 mutation is by itself sufficient to cause ALS in some other special mice.
https://www.jneurosci.org/content/28/9/2075.short
So much technojive, hard for me to figure out whats going on there.
But there does seem to be some debate as to whether SOD1 mutation inside of a single neuron, without interaction with any other cells, just one cell by itself, is sufficient to cause ALS in these mouse experiments.
The other theory seems to be that the mutant SOD1 proteins get outside of the originating cell and interact with "microglia" cells.
"Microglia" is another name for "macrophages that live in the brain."
And then of course LL has a shot at fixing this, either by restricting the movement of the brain macrophages or by repolarizing them.
This 2001 article says mutant SOD1 is not sufficient for ALS in some special mice.
https://www.jneurosci.org/content/21/10/3369.short
Then in 2008 this article with exactly the opposite claim, that SOD1 mutation is by itself sufficient to cause ALS in some other special mice.
https://www.jneurosci.org/content/28/9/2075.short
So much technojive, hard for me to figure out whats going on there.
But there does seem to be some debate as to whether SOD1 mutation inside of a single neuron, without interaction with any other cells, just one cell by itself, is sufficient to cause ALS in these mouse experiments.
The other theory seems to be that the mutant SOD1 proteins get outside of the originating cell and interact with "microglia" cells.
"Microglia" is another name for "macrophages that live in the brain."
And then of course LL has a shot at fixing this, either by restricting the movement of the brain macrophages or by repolarizing them.
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