Jlang, ALS and AD are not homogenous, but neith

Jlang,

ALS and AD are not homogenous, but neither are cancers. As with cancer, it appears there is a therapeutic window in which leronlimab may be beneficial for ALS.

While not addressing the myriad of underlying pathologies (SOD1/FUS/TDP43 proteins, mitochondrial dysfunction, calcium transport pathologies), leronlimab may very well reduce the microglial and macrophage mediated secondary inflammation.

As I'm sure you've found, stable/slowly progressing ALS is associated with a robust population of Tregs (expansion of that population an actively explored therapeutic target). Diminution of that population is correlated with disease progression.

Leronlimab may slow the trafficking of macrophages and activation of microglia, just as is suggested in progression of AD and PD. Obviously all theoretical until proven, but not fanciful.

Cancer at one point believed all driven by genetic mutation, but despite the promised of CRISPR, successful treatment thus far mostly driven by immune modulation.

Fingers crossed that the same success will be seen in these neurologic diseases.