While these data clearly reveal a critical role of POLβ in AD pathogenesis, reduction of POLβ alone is not sufficient to initiate AD; POLβ+/− mice express POLβ at a comparable level at 6 month old and a reduced level at 14 month old compared to 3xTgAD mice, the latter genotype mice develop AD pathology [149]. Here, POLB is linked to Alzheimer disease.