Studies have suggested that Alzheimer's disease (AD) is related to changes in brain function that are present already at very early, pre-clinical stages of the disease. For example, recent functional neuroimaging studies have shown early alterations in brain connectivity, and that these alterations are most prominent in highly-connected cortical "hub areas". These hub areas are also those that are most affected by AD lesions. These findings support the view that AD pathology could, at least in part, result from an activity-dependent degeneration. Initial excessive neural firing in hub areas due to increased excitability or connectivity could lead to later neurodegeneration and disruption of connectivity. Very recently, studies conducted by Prof. JN Octave (UCL) have suggested that AD could be related to a decrease in the expression of the cellular Cl- ion extruder KCC2, leading to an increase in intracellular Cl- and, thereby, an inhibitory-to-excitatory shift of GABAA receptor activity. The aim of my project was to test whether GABAergic neurotransmission is altered at early pre-clinical and pre-demential stages of AD as compared to matched healthy controls.