This working model is consistent with human data showing that cognitive operations dependent on the dlPFC are impaired by stress exposure via β-AR stimulation.47 As stress exposure is a risk factor for multiple neuropsychiatric disorders, including schizophrenia48 and AD,9,49,50 this working model may help to explain why increased risk of neuropsychiatric disorders is consistently associated with alterations in CACNA1C. This evidence concerns the gene CACNA1C and Alzheimer disease.