Which mechanism best describes riluzole's action in ALS?

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In ALS, motor neuron death is tied to glutamate-induced excitotoxicity, and riluzole helps by dampening this process. It mainly reduces presynaptic glutamate release by lowering neuronal excitability through blockade of voltage-gated sodium channels, so less glutamate enters the synapse. With less glutamate around, overactivation of postsynaptic glutamate receptors is reduced, limiting calcium influx and neuronal injury. Some additional effects may include promoting glutamate uptake by astrocytes, but the key clinical point is less glutamate-driven damage. The other drugs listed act on different targets—baclofen for spasticity via GABA-B pathways, gabapentin on calcium channels to modulate excitatory release for neuropathic issues, and memantine as an NMDA antagonist used in other conditions—so riluzole’s mechanism of reducing glutamate excitotoxicity best fits ALS.