Glutathione (GSH) for ALS
Also known as: GSH, L-Glutathione, Reduced glutathione
Motor neurons have limited antioxidant capacity, and GSH depletion accelerates oxidative motor neuron damage in ALS.
Mechanism of Action
GSH neutralizes superoxide, hydrogen peroxide, and lipid peroxides in motor neurons. It detoxifies electrophilic xenobiotics, maintains redox-sensitive protein function, and supports mitochondrial membrane integrity. SOD1-mutant ALS shows accelerated GSH consumption.
General mechanism: Tripeptide antioxidant (γ-glutamyl-cysteinyl-glycine). Master cellular redox regulator, detoxification conjugate, immune modulator.
Current Evidence
CSF and blood GSH levels are reduced in ALS patients. Direct supplementation trials are limited due to poor oral bioavailability. IV and liposomal formulations being explored.
Clinical Status: Biomarker data strong. Delivery challenges. No definitive ALS trials.
Safety Profile
Very safe. Poor oral bioavailability (IV, liposomal, intranasal preferred). No significant side effects at therapeutic doses.
Key Research Questions
- Can liposomal GSH achieve motor neuron protection?
- Does GSH combination with NAC provide sustained antioxidant defense in ALS?