This paper extends the unified G₀ and ΔGd cellular framework from the preceding SFL-CELL papers to interpret the core pathogenesis of amyotrophic lateral sclerosis (ALS). Motor neurons possess a specialized complete G₀ architecture containing dedicated modules for axon repair, signal conduction and metabolic self-maintenance. ALS does not stem from random neuronal immune attack or de novo toxic mutation; it originates from continuous accumulation of irreversible ΔGd(-) impairment that gradually dismantles each functional segment of the neuron’s native G₀ structure. Universal state equation consistent with the whole SFL serial system G = G₀ + ΔGd(+) − ΔGd(−) Mild daily physiological wear ΔGd(+) can be fully offset by the neuron's baseline metabolic repair capacity and will not trigger persistent functional decline. Long-term oxidative stress, inflammatory circulation and chronic micro-tissue damage keep adding permanent ΔGd(−) loss. As the intact baseline value G of motor neurons falls steadily, axonal repair efficiency declines sharply, nerve signal transmission becomes unstable, and muscle innervation gradually fails, producing progressive weakness, atrophy and paralysis. The progressive deterioration of ALS reflects the sequential collapse of independent functional modules within the original fixed G₀ framework, rather than cells acquiring degenerative traits autonomously. Current symptomatic treatments only alleviate late-stage manifestations, while the fundamental intervention target should be reducing ΔGd(-) accumulation and preserving the complete native G₀ structure of motor neurons. This degenerative damage pathway aligns with the unified cellular pathology of SLE and malignant proliferation laid out earlier, and its long-term systemic consumption effect can be quantified with the lifespan formula in the subsequent SFL-LS serial.
FOO SENG ANG (Sat,) studied this question.