Alzheimer’s disease is driven by converging pathological processes, including amyloid-β accumulation, tau dysfunction, synaptic failure, and chronic neuroinflammation, which emerge decades before clinical onset. Growing evidence supports the concept that early, upstream neuroprotective interventions may meaningfully alter disease trajectory in both sporadic and familial AD. Taurine, an endogenously abundant and clinically safe neuromodulator, has re-emerged as a promising multi-target regulator of AD-relevant pathways. Accumulating mechanistic data indicate that taurine modulates Aβ aggregation, attenuates oxidative and endoplasmic reticulum stress, preserves mitochondrial homeostasis, suppresses neuroinflammatory signaling, and stabilizes synaptic function, positioning it as a promising upstream intervention strategy in AD. This review synthesizes current evidence supporting taurine’s pleiotropic neuroprotective actions and discusses its translational potential as an early-stage, low-risk intervention to delay or prevent AD progression.
Hossain et al. (Sun,) studied this question.