Glutathione (GSH) for Alzheimer's Disease
Also known as: GSH, L-Glutathione, Reduced glutathione
Brain GSH depletion correlates with cognitive decline and may precede clinical Alzheimer's symptoms.
Mechanism of Action
GSH protects neurons from amyloid-beta-induced oxidative damage, detoxifies lipid peroxidation products (4-HNE, MDA), and maintains redox-sensitive signaling essential for synaptic plasticity. It also supports detoxification of aluminum and mercury that may contribute to AD pathology.
General mechanism: Tripeptide antioxidant (γ-glutamyl-cysteinyl-glycine). Master cellular redox regulator, detoxification conjugate, immune modulator.
Current Evidence
MRS studies show reduced brain GSH in MCI and AD. Correlation between GSH levels and cognitive scores documented. Supplementation studies limited by delivery challenges.
Clinical Status: Biomarker correlation established. Supplementation trials limited.
Safety Profile
Very safe. Poor oral bioavailability (IV, liposomal, intranasal preferred). No significant side effects at therapeutic doses.
Key Research Questions
- Can intranasal GSH restore brain redox balance in early AD?
- Does brain GSH level predict AD progression rate?