However, in the current investigation, the observed upregulation of AA uptake and increased expression levels of both SVCT1 and SVCT2 in the jejunum of 5xFAD mice compared to WT littermates suggest that these animals were undergoing oxidative stress owing to their AD pathology and, consequently, depleting vitamin C levels in this important organ triggered a compensatory response. The gene discussed is SLC23A1; the disease is Alzheimer disease.