Wake, sleep and circadian disturbances are common occurrences in Alzheimer’ disease (AD) and other tauopathies often preceding disease-defining symptoms. Clinical data point to a divergent sleep-wake behavior profiles among tauopathies which probably reflects their differential pattern of neuronal vulnerability and spread and thus, have implications for developing symptomatic and disease-modifying treatments. Although some aspects of the neurobiological basis of sleep disturbances in neurodegenerative diseases have been studied, including the bidirectional relationship between sleep apnea and beta-amyloid levels and more recent a possible impact of lack of sleep in tau levels, other aspects remain underexplored.