BBB damages caused by dysfunctional cellular components, such as β-catenin-mediated CLDN3 downregulation, are known to be related to the onset and progression of various neurological diseases, including stroke, multiple sclerosis, epilepsy, and Alzheimer’s disease [48, 49, 56, 57]. This evidence concerns the gene CLDN3 and early-onset autosomal dominant Alzheimer disease.