Sleep and Neurological Diseases and Disorders Across the Life Span

Abstract

Sleep is an essential pillar of health at every stage of life, and even a single night of poor sleep can produce measurable cognitive deficits. Chronic sleep disturbances are increasingly linked to neurological disorders, including Autism Spectrum Disorder (ASD), Schizophrenia (SCZ), and Alzheimer’s Disease (AD), where underlying causes remain incompletely understood. Converging evidence indicates that sleep disruption, together with gene mutations affecting synaptic function, interferes with homeostatic processes that stabilize neural circuits. This review examines how alterations in sleep timing, duration, and architecture impair synaptic plasticity, particularly the balance between Hebbian and homeostatic mechanisms. Across ASD, SCZ, and AD, persistent and non-restorative sleep disturbances are associated with circadian dysregulation, reduced slow-wave activity and sleep spindles, and impaired synaptic downscaling. These disruptions contribute to disorder-specific outcomes, including behavioral dysregulation in ASD, psychosis, and cognitive impairment in SCZ, and neurodegeneration and β-amyloid accumulation in AD. Shared molecular pathways, including NMDA receptor dysfunction, GABAergic imbalance, and mutations in synaptic proteins such as SHANK3, further link sleep abnormalities to disease progression. The bidirectional relationship between sleep and pathology suggests that sleep disturbance both reflects and drives neurological dysfunction. Together, these findings highlight sleep as a central mechanism in synaptic stability and a promising target for therapeutic strategies across multiple neurological disorders.