|cell-cell junction organization can be categorized into adherens and tight junction interactions. These interactions connect neighbouring cells and links intracellularly to the actin cytoskeleton and signalling pathways. Tight junction is composed of transmembrane proteins, holding adjacent cells in close contact, controlling paracellular permeability thus forming barrier. Tight junction is typical of epithelial cells, but can be formed by endothelial cells as well. Adherens junction is multi-protein complexes that promotes homotypic cell adhesion in almost all types of tissues. Adherens junction also binds directly to cytoplasmic proteins, which regulate the organization of cytoskeleton, and signalling events. Adherens junction also regulates cell polarity and shape (Hartsock & Nelson, 2008).|
|Involvement in Alzheimer's disease|
It has been proposed that inflammation and blood-brain barrier dysfunction are crucial in AD pathogenesis (Stolp & Dziegielewska, 2009; Ujiie, Dickstein, Carlow, & Jefferies, 2003). The abnormalities of endothelial tight junction has been observed in brain biopsies from AD patients (Stewart & Hayakawa, 1992). It seems that Abeta 1-42 can cause relocation and affect expression of tight junction proteins (Marco & Skaper, 2006), thus disrupting the integrity of blood-brain barrier.
There are very few studies on involvement of adherens junction in AD. Two genes, PVRL2 and FERMT2, showed significant variation in GWAS studies, are both involved in adherens junction organization pathway(Harold et al., 2009; Lambert et al., 2013).