Amyloid precursor protein-Tau interaction

The **Amyloid precursor protein-Tau interaction** refers to the direct and indirect molecular contacts between APP (and its cleavage product amyloid-β, Aβ) and tau protein, both of which are central to the pathology of Alzheimer’s disease. APP is cleaved to form Aβ, which facilitates phosphorylation and aggregation of tau. Experimental studies show these proteins interact at specific epitopes to promote each other's misfolding and aggregation, leading to synaptic dysfunction, neurodegeneration, and cognitive impairment. Targeting their interaction has emerged as a promising therapeutic strategy, with the aim of preventing the synergistic toxicity that drives disease progression. Although this is not a canonical single-molecule target, inhibitors of the APP-tau interface are under investigation as novel disease-modifying therapeutics for Alzheimer's disease[1][2][3][4][6]. **Note:** For structured database purposes, this entry should be flagged as a *non-standard target* (protein-protein interaction, not a single gene/protein) and mapped to its constituent proteins wherever possible.

Other names

APP-Tau interactionAβ-Tau interaction (when referring to interaction of amyloid-β, the APP cleavage product, with tau)Amyloid-beta–tau cross-seeding

Inhibition of protein-protein interaction (e.g., peptides blocking APP-tau binding)[2][3] Disruption of cross-seeding to prevent aggregation of Aβ and phosphorylated tau[3][6] Modulation of kinases/phosphatases phosphorylating tau (downstream effect)[1]