Excitotoxicity plays a key role in the selective vulnerability of striatal neurons in Huntington disease (HD). Decreased glutamate uptake by glial cells could account for the excess glutamate at the synapse in patients as well as animal models of HD. The major molecule responsible for clearing glutamate at the synapses is glial glutamate transporter GLT-1. https://www.roneverhart.com/Wacoal-Women-s-Awareness-Unlined-Full-Figure-Underwire-Bra-Ivory-36DD/
Palmitoylation and function of glial glutamate transporter-1 is reduced in the YAC128 mouse model of Huntington disease
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