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Insulin-like growth factor-1 and cognitive health: Exploring cellular, preclinical, and clinical dimensions
Cellas A Hayes1, Destiny Wilson2, Miguel A De Leon2
1Department of Epidemiology and Population Health, School of Medicine, Stanford University, Stanford, CA 94305, USA; Department of Biomolecular Sciences, School of Pharmacy, University of Mississippi, University, MS 38677, USA.
Abstract:
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.
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