Sleep is an essential requirement of all animal life, including humans, who spend around a third of their life asleep. It is controlled by an internal biological clock, our circadian rhythm, which controls the timing of when we rest, sleep, and are active. We do not understand why humans need to sleep, however, it is becoming clear that sleep and circadian rhythms are linked to cognition (brain functions such as thinking and memory). Sleep and circadian rhythms are disrupted in neurological diseases where the brain is gradually damaged over time, called neurodegenerative diseases. These diseases include Alzheimer's disease, the most common cause of dementia worldwide and a leading cause of death. Alzheimer's disease causes alterations in sleep and circadian rhythms. These changes can occur before other symptoms and may help us identify those who will develop these diseases. Early diagnosis is essential as it enables treatment before damage to the brain is too widespread. Evidence is also emerging that abnormal sleep and circadian rhythms may be part of the cause of Alzheimer's disease. We do not know why abnormal sleep and circadian rhythms emerge, how they change over time, or how they relate to cognition in the long term. It is unclear if disturbed circadian rhythms are early signs of disease, or if they precede and cause neurodegenerative diseases. To answer these questions we must analyse sleep and circadian rhythms in detail. Bed mats placed under the mattress, and worn devices, called actigraphy, allow us to closely monitor sleep and circadian rhythms in patients' own homes. The genes and sleep-promoting chemicals which control sleep and circadian rhythms can be detected in the blood and spinal fluid. Advanced brain imaging, blood and spinal fluid analysis allows us to detect signs of damage and neurodegenerative diseases in the brain. The Medical Research Council National Survey for Health and Development (NSHD) offers a unique opportunity to examine the effects of abnormal sleep and circadian rhythms on cognition and neurodegenerative disease. It has followed 5362 people born in Britain on the same week in 1946, with regular questionnaires throughout their lives. The Insight 46 study has recruited is recruiting a further 872 people from NSHD to have advanced brain imaging, detailed cognitive assessments, actigraphy, genetic testing, and sampling of their blood and spinal fluid to analyse for evidence of neurodegeneration. 250 people will undergo repeat assessments, and 100 will have at least 6 months of bed mat analysis. These repeated and prolonged assessment allow particularly detailed examination of changes in sleep and circadian rhythms over time, and how they relate to progressive changes in cognition, brain imaging, and in the blood or spinal fluid. We will also examine the chemicals that control sleep and circadian rhythms in the spinal fluid of 375 participants, and examine how the genes that control sleep or make you more likely to develop Alzheimer's disease relate to sleep, circadian rhythms, and signs of neurodegenerative disease in old age. One fifth of those within Insight 46 already have early signs of Alzheimer's disease. For my PhD I plan to examine how sleep and circadian rhythms relate to cognition and neurodegenerative disease. Using sleep and circadian rhythm questionnaire data from birth to the seventh decade with sleep data from actigraphy and bed mats, I will examine sleep and circadian rhythms over the human lifetime in unparalleled detail. Combining this with the advanced brain imaging, cognitive, blood and spinal fluid data already collected from Insight 46 will allow me to explore how sleep and circadian rhythms relate to cognition and neurodegenerative disease. Finally, I will examine how this process is controlled by our genes, and sleep promoting chemicals, and whether failures in this control system are related to cognition and neurodegenerative disease.