Insulin-like growth factor-1 and cognitive health: Exploring cellular, preclinical, and clinical dimensions

•Aging is the primary risk factor for cognitive impairment and dementia.•Insulin-like growth factor 1 (IGF-1) declines throughout lifespan.•In preclinical studies, the reduction in IGF-1 is associated with reduced cognitive performance.•In clinical cohorts, lower IGF-1 is associated with increased cognitive impairment.•IGF-1 has pleiotropic neuroendocrine signal functions in neurons and neuroglia that contribute to its beneficial effects on cognition. Age and insulin-like growth factor-1 (IGF-1) have an inverse association with cognitive decline and dementia. IGF-1 is known to have important pleiotropic functions beginning in neurodevelopment and extending into adulthood such as neurogenesis. At the cellular level, IGF-1 has pleiotropic signaling mechanisms through the IGF-1 receptor on neurons and neuroglia to attenuate inflammation, promote myelination, maintain astrocytic functions for homeostatic balances, and neuronal synaptogenesis. In preclinical rodent models of aging and transgenic models of IGF-1, increased IGF-1 improves cognition in a variety of behavioral paradigms along with reducing IGF-1 via knockout models being able to induce cognitive impairment. At the clinical levels, most studies highlight that increased levels of IGF-1 are associated with better cognition. This review provides a comprehensive and up-to-date evaluation of the association between IGF-1 and cognition at the cellular signaling levels, preclinical, and clinical levels.