GPR68 and Alzheimer disease: We speculated that HIIT ameliorates AD pathology by mitigating stressors such as acidosis and inflammation (Yu et al., 2025), which would otherwise sustain compensatory GPR68 upregulation.​​ This implies that prolonged GPR68 activation is unnecessary, ​​given its dual roles: activation in acidic microenvironments (Ludwig et al., 2003) and induction of pro-inflammatory cytokine release (Ichimonji et al., 2010).