SLCO1C1 encodes OATP1C1, a sodium-independent organic anion transporter that mediates high-affinity transport of thyroid hormones across cell membranes 1. The transporter specifically recognizes thyroxine (T4), T4 sulfate, and reverse T3, with much lower efficiency for triiodothyronine (T3) and estrogen metabolites 2. In the brain, SLCO1C1 facilitates thyroid hormone delivery across the blood-brain barrier and regulates regional T4 levels by transporting T4 and serving as an export pump for T4 sulfate, which can be hydrolyzed to regenerate T3 locally 3. Notably, SLCO1C1 is coexpressed with deiodinase 2 in outer radial glia and astrocytes, suggesting coordinated regulation of local T3 formation crucial for neurogenesis 3. Disease relevance includes OATP1C1 deficiency, which causes brain hypometabolism and progressive neurodegeneration 1. Recent exome-wide association studies identified SLCO1C1 as a novel gene associated with Alzheimer's disease and related dementia risk 4, suggesting therapeutic potential as a drug target. Additionally, prenatal PFAS exposure is associated with decreased placental SLCO1C1 methylation, which mediates adverse effects on fetal thyroid hormone levels 5.