Inflammatory cells are a medium that allows the generation of...

Inflammatory cells are a medium that allows the generation of negative cells.
If you take away or decrease inflammation in particular areas you diminish the opportunity for negative cell growth.
Oxidative damage is high in ALS, you want it low.
Inflammation aids oxidative outcomes via various mechanisms.

Below touches on the complex mechanisms.

"We sought to demonstrate that CEP accumulation serves as a readout of oxidative stress in the brain. The main findings from the study are: (1) inflammatory cells generate CEP from PUFA peroxidation as activation-dependent and MPO-mediated process. (2) CEP accumulates in ALS patients' brains at high level, particularly in the SOD1-type ALS cases, and is co-localized with inflammatory and MPO-expressing cells. (3) CEP is present in major cell types which contribute to ALS pathogenesis, including astrocytes and microglia. However, only in SOD1-type ALS cases CEP is accumulated in neurons.
CEP was reported to be involved in inflammation-associated pathologies, including atherosclerosis, hyperlipidemia, thrombosis, macular degeneration and tumor progression [7]. More mechanistic studies revealed that CEP promotes macrophage adhesion to the extracellular matrix and their migration to the inflamed site [9,18], polarization toward the pro-inflammatory M1 phenotype [27,28], and expression of pro-inflammatory cytokines [28]. The level of CEP in pathological processes is well-regulated. For example, the fluctuation of CEP levels adopts a bell-shaped pattern during wound healing. At the early stage of wound healing, CEP is generated rapidly and heavily deposited in wound tissue. CEP level returns to normal when the wound is healed [11]. CEP can be recognized, scavenged, and cleared by macrophages, preferentially and more effectively by M2 macrophages [10]. Collectively, these data indicate that endogenous levels of CEP is tightly coupled with and regulated by inflammation."