CACNA1C and Cognitive impairment: Singhal K and Sandhir R [28] reported elevated Cav1.2 mRNA and protein levels in the brains of diabetic mice, leading to exaggerated synaptic Ca2+ influx; the L-type Ca2+ channel blocker nimodipine normalized Cav1.2 expression, restored Ca2+-dependent synaptic plasticity, and reversed cognitive deficits.