However, a recent report indicated that inflammation either mediated by IL1β or in an EAE model induces the expression of TJ proteins at the GL level, strengthening the GL barrier against immune cell penetration; (2) Proteins implicated in β-amyloïd clearance by astrocytes [40,41] suggesting a possible protective effect against Alzheimer disease as recently reported [42]; (3) Ion transporters which could compensate for ionic homeostasis modification induced by Cx43 gap junctions and hemichannels depletion. Here, GJA1 is linked to Alzheimer disease.