Neurological disorders as diverse as multiple sclerosis (MS), Alzheimer’s disease (AD), and Huntington´s disease (HD) are characterized by a functional impairment of neural circuits underlying cognitive and motor functions. Although demyelination and axonal damage or neuronal and synapse loss are central in the pathophysiology, early neuronal network dysfunctions, representing new allostatic set points on network level and often preceding behavioral symptoms or neurodegeneration have a significant contribution to disease burden, they may even represent a pathology in itself, only indirectly mediated by initial pathological insult. We are studying cortical functional networks in rodents in vivo by combining state-of-the-art optogenetic techniques with optical calcium imaging and fMRI, with a focus on slow oscillations, for a causal understanding of the relevance of these early network dysregulations.
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