Abstract: Huntington’s disease (HD) is a progressive neurodegenerative disorder characterized by selective
striatal neuronal loss, motor impairment, cognitive decline, and psychiatric disturbances. A central driver of
neuronal vulnerability in HD is excitotoxicity, wherein excessive glutamatergic signaling induces pathological
activation of NMDA receptors, intracellular calcium overload, mitochondrial dysfunction, and oxidative stress–
mediated cell death. Although symptomatic treatments exist, disease-modifying strategies remain limited.
Neuroprotective interventions targeting excitotoxic cascades therefore represent a critical therapeutic priority.
The present investigation adopts a structured translational......
Key Word: Huntington’s disease; excitotoxicity; neuroprotection; NMDA receptor; mitochondrial dysfunction;
oxidative stress; gene-silencing therapy; translational neuroscience; neurodegeneration.
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