Finally, Lack of recovery might be due to the fundamental differences between MS and EAE. This study highlights the need for better preclinical models representing PMS.

Others show ABT-263 improves clinical score, but unclear why it is more effective than DQ. One possibility is that the therapeutic effectiveness of senolytics depends on cell type or pathways targeted, and not all senolytics are equally effective at inducing senolysis.

Previous work from lab show DQ was more effective in enhancing remyelination in young vs aged mice, suggesting other inflammatory factors may be inhibiting remyelination. So ongoing inflammatory environment observed in EAE,much like aged tissue may limit DQ therapeutic efficacy.

We show SC myeloid cells accumulate in spinal cord lesions and leptomeningeal compartment following EAE. We also show senescence gene signature increases w disease progression. However, SC reduction does not improve EAE outcome. Few important conclusions made from this work: