In this review, we outlined the role of aberrant synaptic plasticity in the aetiology of AD (predominantly amyloid β‐driven and to a lesser extent tauopathy‐driven) and dived into the role of GluA1 in synaptic plasticity, in the hippocampus as it pertains to induction and maintenance of LTP and LTD (Figure 1). Here, GRIA1 is linked to tauopathy.