Magnesium L-Threonate (MgT) for ALS
Also known as: MgT, Magtein, MMFS-01
Brain and spinal cord magnesium deficiency may contribute to glutamate excitotoxicity in ALS motor neurons.
Mechanism of Action
Mg²⁺ blocks NMDA receptor channels in a voltage-dependent manner, providing natural protection against glutamate excitotoxicity. MgT-mediated CNS Mg²⁺ elevation may complement riluzole's anti-glutamate mechanism and support motor neuron viability.
General mechanism: BBB-penetrant magnesium salt. Elevates brain Mg²⁺ for NMDA receptor modulation, synaptic density enhancement, BACE1 suppression.
Current Evidence
No ALS-specific clinical trials. Rationale based on excitotoxicity mechanism and CNS penetration. Preclinical studies on neuronal protection supportive.
Clinical Status: No ALS trials. Mechanistic rationale strong.
Safety Profile
Very safe. Mild GI effects. No significant interactions. Well-tolerated at recommended doses.
Key Research Questions
- Does CNS Mg²⁺ elevation reduce excitotoxic motor neuron damage?
- Can MgT synergize with riluzole for anti-excitotoxic neuroprotection?