During the pre-clinical stages of Alzheimer’s disease, i.e. when subtle changes are taking place in the brain but no cognitive symptoms can be observed, the cortex presents a state of transient hyperexcitability. To date, several studies conducted in animals have shown that tau and beta-amyloid proteins—central to the development of Alzheimer’s disease—were associated with increased cortical excitability and dysfunction of brain networks. However, the relationship between the accumulation of Alzheimer’s disease-related proteins and cortical hyperexcitability during the earliest stages of the disease remains poorly understood in humans, in particular due to technological limitations in the precise quantification of early protein deposition.