The relationship between calbindin and tau pathology was directly studied in the dlPFC of patients with AD, where it was found that the layer III pyramidal cells in the dlPFC that express calbindin when younger and healthy are especially vulnerable to tau pathology and degeneration, while interneurons retained calbindin expression and did not degenerate (Hof and Morrison, 1991). This evidence concerns the gene CALB1 and Alzheimer disease.