Alzheimer's dementia (AD) is a neurodegenerative disease that is often accompanied by severe sleep disturbances. The manifestation of the sleep disturbances is twofold: nighttime hyperarousal sometimes accompanied by irritability and agitation, and daytime excessive sleepiness. Thus, although treatment with sedatives or hypnotics may offer some relief to the nighttime hyperarousal, the daytime excessive sleepiness remains mostly unresolved. Recently, however, more promising results in relief of excessive daytime sleepiness, as well as nighttime hyperarousal, are offered by the chronobiological approach. This approach attributes the sleep problems of AD patients to a dysfunction in a broader neuronal mechanism, namely the biological clock, that paces various physiological functions, among which is the sleep-wake cycle. The biological clock, situated in the suprachiasmatic nuclei (SCN) of the hypothalamus, receives environmental light input via neuronal signals from the retina. The SCN, in turn, innervates the pineal gland, that is responsible for the production and release of melatonin. Light stimulus causes the attenuation of melatonin secretion from the pineal gland; whereas the cessation of light increases melatonin secretion. In diurnal mammals, the dim light melatonin onset (DLMO) is in accordance with sleep onset. The chronobiological approach offers two main treatments to the sleep problems in AD patients: morning exposure to bright light and evening administration of melatonin, both of which show at least moderate success in restoring the sleep-wake cycle in AD patients, that is more marked in the early stages of the disease.