Agree there are/could be multiple etiologies behin
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Posted On: 11/08/2021 12:42:25 PM
Agree there are/could be multiple etiologies behind the "syndrome" of ALS, with final stage the death of motor neurons. I do think that multiple lines of evidence point to the importance of astrocytes. Will be watching these Kadimastem trials of intrathecal astrocyte cell therapy closely.
https://www.frontiersin.org/articles/10.3389/...00824/full
Too bad the Brainstorm "NurOwn" trials (stem cells to secrete neurotrophic factor) failed in P3 for ALS.
I was always fascinated about all the "junk" DNA in our genomes (up to 10%?) inserted there by these retroviruses, which then are passed on forever. Who knows if any of the remnants are "intact," how they reactivate, and what havoc they may cause. HERVs could also play prominent role in other CNS diseases like MS. HERV-K was found in just a subset of ALS patients.
As we figure out the etiologies better, we will likely have subsets of disease, such as ALS-HERV, ALS-C9Orf72, PD-parkin, etc... with different treatments for each.
It's too bad all of these animal models haven't resulted in finding good treatments for human neurodegenerative diseases. But, we have to keep trying.
I'm a big fan of supporting the mitochondria (antioxidants, and increasing the ratio of NAD+/NADH via NR or other supplements), neurotrophic secreting cell therapy, and astrocyte replacement cell therapy for ALS, all to try to keep the motor neurons well supported and alive.
We do need better understanding of the interaction of the immune system with glial cells and neurons in all these CNS diseases. Leronlimab could play a role in dampening down the immune system and preventing or slowing neurodegeneration in general, especially those with an autoimmune component like MS. But there is a lot to learn, and LL is not likely one molecule that treats everything, especially, as you say, for all these poorly understood, heterogenous CNS diseases like ALS.
https://www.frontiersin.org/articles/10.3389/...00824/full
Too bad the Brainstorm "NurOwn" trials (stem cells to secrete neurotrophic factor) failed in P3 for ALS.
I was always fascinated about all the "junk" DNA in our genomes (up to 10%?) inserted there by these retroviruses, which then are passed on forever. Who knows if any of the remnants are "intact," how they reactivate, and what havoc they may cause. HERVs could also play prominent role in other CNS diseases like MS. HERV-K was found in just a subset of ALS patients.
As we figure out the etiologies better, we will likely have subsets of disease, such as ALS-HERV, ALS-C9Orf72, PD-parkin, etc... with different treatments for each.
It's too bad all of these animal models haven't resulted in finding good treatments for human neurodegenerative diseases. But, we have to keep trying.
I'm a big fan of supporting the mitochondria (antioxidants, and increasing the ratio of NAD+/NADH via NR or other supplements), neurotrophic secreting cell therapy, and astrocyte replacement cell therapy for ALS, all to try to keep the motor neurons well supported and alive.
We do need better understanding of the interaction of the immune system with glial cells and neurons in all these CNS diseases. Leronlimab could play a role in dampening down the immune system and preventing or slowing neurodegeneration in general, especially those with an autoimmune component like MS. But there is a lot to learn, and LL is not likely one molecule that treats everything, especially, as you say, for all these poorly understood, heterogenous CNS diseases like ALS.
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