Although this transition at the molecular level is revealed, experimentally accessible, and tunably controllable under conditions far from physiological, it is parallel, and may be mechanistically related, to one of the multiple, critical transitions or tipping points, between the prospects for human long-term health, survival, dementia, and death from Alzheimer’s disease and related tau amyloid-associated neurodegenerative pathologies. The gene discussed is MAPT; the disease is early-onset autosomal dominant Alzheimer disease.