Beyond genetic subtypes that affect the course of early onset AD, Schneider and colleagues [4] have also suggested that older participants with probable AD might have non-Alzheimer neuropathology (e.g., vascular disease, hippocampal sclerosis, TDP-43 proteinopathy) and/or decline more slowly than younger participants because of survival bias by which more rapidly declining individuals have progressed to a point where they are no longer eligible for the studies. The gene discussed is TARDBP; the disease is Alzheimer disease.