This project aims at causally investigating an oscillatory neuronal population activity highly relevant to maintaining cognitive function: the slow oscillation. Slow oscillations represent a characteristic feature of non-REM sleep, and play a major role in memory consolidation. Slow oscillations propagate as a travelling wave, as observed both in human and animal studies. In a recent study of ours we showed that a causal optogenetic probing of travelling slow waves is feasible, in combination with optic-fiber-based Ca2+ recordings. But why are slow oscillations implicated in neurodegenerative disorders? Alzheimer's disease patients experience striking fluctuations in memory functions, often within the same day. It is unlikely that changes in synapse or nerve cell numbers due to amyloid deposition account for these. Instead it has been proposed that they reflect variations in the activity of the neuronal network. Just recently, a link between the dysregulation of slow oscillations in a rodent model of AD, normal network function and behavior was suggested. Notably, resting state fMRI data indicates an impairment of large-scale oscillations in AD patients. Causally investigating key features of slow oscillations including clinically applicable imaging methods will not only further our understanding of network impairment and disease mechanisms, but might also link human neuroimaging data with highly spatio-temporally resolved experimental methods. However, for that, we need to develop and apply a novel combination of four key methods: 1) applying fast sequences in fMRI to resolve a travelling wave with a velocity of about 30 mm/s; 2) Developing novel opto-acoustic methods to complement the fMRI approaches, with the potential of an even faster readout, 3) Combining fMRI and optoacoustic approaches with optic-fiber based optogenetics and neuronal Ca2+ recordings, in a closed-loop approach.