The Neuroprotective Mechanism of Gastrodin in the Intervention of Alzheimer's Disease

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the core pathological features of β-amyloid (Aβ) deposition and excessive phosphorylation of Tau protein. Its pathological changes can induce oxidative stress, neuroinflammation and neuronal apoptosis, ultimately leading to cognitive dysfunction. Gastrodin, as the main active component of the traditional Chinese medicine Gastrodia elata, has attracted extensive attention due to its good blood-brain barrier penetration ability and multi-target neuroprotective effects. This article systematically reviews the molecular mechanisms and preclinical research evidence of gastrodin in the intervention of AD. At the molecular level, gastrodin exerts antioxidant stress, inhibits neuroinflammation, blocks neuronal apoptosis and protects the blood-brain barrier by regulating multiple signaling pathways. Animal experiments have shown that gastrodin can effectively reduce Aβ deposition and Tau protein phosphorylation, improve mitochondrial energy metabolism, and significantly enhance the learning and memory ability of AD model animals. In conclusion, gastrodin exerts neuroprotective effects through a multi-target network system of "antioxidant-anti-inflammatory-anti-apoptotic", showing great potential as an innovative drug for AD or a neuroprotective agent.