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RESEARCH PAPER / 2024-11-14

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

Cellas A Hayes, Destiny Wilson, Miguel A De Leon, Mubarak Jolayemi Mustapha, Sharon Morales, Michelle C Odden, Nicole M Ashpole

Department 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. Electronic address: [email protected]. · pubmed

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.

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper discusses the role of IGF-1 in cognitive health, particularly its cellular mechanisms and associations with cognitive decline, which are relevant to understanding aging processes. However, while it provides a solid review of existing literature, it does not present novel findings or significant advancements that would greatly impact the field of longevity research. The focus remains on associations rather than addressing root causes or mechanisms of aging directly.

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