Insomnia and Cognitive Functions: Focus on Neurobiological Mechanisms

Insomnia is the most prevalent sleep disorder worldwide, affecting up to 30% of the population, and is frequently accompanied by cognitive complaints and measurable cognitive impairments. Chronic insomnia is characterized by persistent hyperarousal across physiological, cognitive, and neurobiological domains, which may compromise multiple cognitive systems. This review synthesizes current evidence on the impact of insomnia on major cognitive domains, including attention, language, memory and learning, executive functions, perceptual–motor skills, and social cognition. We critically evaluate methodological factors contributing to heterogeneous findings across studies, such as variability in diagnostic criteria, insomnia phenotypes, cognitive assessments, and sample characteristics. Additionally, we summarize emerging evidence on neuroanatomical and molecular correlates of insomnia-related cognitive impairment, including alterations in hippocampal and prefrontal brain structures, amyloid-β accumulation, dysregulation of brain-derived neurotrophic factor, neurotransmitter imbalance, neuroinflammation, and disrupted signaling pathways. Insights from preclinical studies show mechanistic links between sleep loss, synaptic dysfunction, oxidative stress, and memory decline. Despite substantial advances, the precise pathophysiological mechanisms underlying cognitive dysfunction in insomnia remain incompletely understood, suggesting that cognitive impairment arises from the convergence of multiple biological processes rather than a single causal pathway. A deeper mechanistic understanding is essential for developing targeted interventions for preventing cognitive decline in individuals with insomnia.