Figure 1: Molecular signalling involved in amyloid β (Aβ)-mediated synapse loss in Alzheimer’s disease. In dendrites, accumulation of Aβ leads to mitochondrial stress, cytochrome c release, and caspase-3 activation. Caspase-3 activates calcineurin, which dephosphorylates AMPARs, leading to their subsequent removal from the post-synaptic density (PSD) and causing dendritic spine degeneration. Caspase-3 is also implicated in tau truncation and activation of GSK-3β. Tau truncation, together with GSK-3β- dependent tau phosphorylation, promotes neurofibrillary tangles (NFTs), contributing to synaptic degeneration.