Skip to main content
Fig. 11 | Acta Neuropathologica Communications

Fig. 11

From: GJA1 (connexin43) is a key regulator of Alzheimer’s disease pathogenesis

Fig. 11

A working hypothesis of GJA1 dysregulation in AD. Progressive upregulation of GJA1 in the brains during LOAD pathogenesis (in response to amyloid accumulation) serves to enhance the coordinated gene network function to orchestrate neuroprotective response by astrocytes including Aβ production and clearance (CST3, CLU, CTSB, ECE2, MEGF10, PSENEN and GSAP), APOE production (APOE, ABCA1, CAV1 and SPON1), and supporting neuronal activity (DLG4, NLGN3, GRINA and GRIN2D). However, the enhanced neuronal activity due to chronic and prolonged GJA1 upregulation triggers neuronal wear and eventual death

Back to article page