SLC17A6 (VGLUT2) is a multifunctional transporter at the synaptic vesicle membrane that loads glutamate into vesicles for release at excitatory synapses. It operates primarily as a uniporter driven by the proton electrochemical gradient established by vacuolar H+-ATPase, transporting L-glutamate and phosphate from the cytoplasm into synaptic vesicles. The transporter also functions as a chloride channel and potassium/proton antiporter to maintain the electrical gradient necessary for sustained glutamate uptake. At the plasma membrane following exocytosis, SLC17A6 acts as a sodium-phosphate symporter contributing to synaptic phosphate homeostasis. SLC17A6 dysfunction is implicated in several neurological disorders. In Alzheimer's disease, SLC17A6 was identified as a hub gene associated with early synaptic abnormality subtypes, with dysregulation observed in the entorhinal cortex of affected patients 12. In Parkinson's disease, a genetic variant (rs1900586) in SLC17A6 demonstrated gene-by-smoking interaction, where the protective effect of smoking against PD was less pronounced in carriers of the minor allele 3. Additionally, reduced SLC17A6 expression in the subthalamic nucleus causes behavioral hyperlocomotion and altered dopaminergic function in mice 4. DNA methylation changes at SLC17A6 are associated with PD in cortical neurons with sex-specific patterns 5. Recent transcriptomic analyses in schizophrenia identified SLC17A6-expressing neuronal subpopulations with putative alterations in proportion and gene activity 6.