OCLN and nervous system disorder: Moreover, the interaction between Aβ and the receptor for advanced glycation end-product (RAGE) suppressed the expression of occludin and elevated the expression of matrix metalloproteinases (MMPs) by mediating the Ca2+- neurocalcin signaling pathway, further damaging the tight junction in the BBB, altered the morphology of brain microvascular, and aggravated the accumulation of Aβ in the brain, indicating that the decreased expression of tight junction proteins induced by T2DM might be responsible for the neurological disorders [10].