Author: ["E. Carro","J.L. Trejo","T. Gomez-Isla","D. LeRoith","I. Torres-Aleman"]
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Abstract
Levels of insulin-like growth factor I (IGF-I), a neuroprotective hormone, decrease in serum during aging, whereas amyloid-β (Aβ), which is involved in the pathogenesis of Alzheimer disease, accumulates in the brain. High brain Aβ levels are found at an early age in mutant mice with low circulating IGF-I, and Aβ burden can be reduced in aging rats by increasing serum IGF-I. This opposing relationship between serum IGF-I and brain Aβ levels reflects the ability of IGF-I to induce clearance of brain Aβ, probably by enhancing transport of Aβ carrier proteins such as albumin and transthyretin into the brain. This effect is antagonized by tumor necrosis factor-α, a pro-inflammatory cytokine putatively involved in dementia and aging. Because IGF-I treatment of mice overexpressing mutant amyloid markedly reduces their brain Aβ burden, we consider that circulating IGF-I is a physiological regulator of brain amyloid levels with therapeutic potential.Cite this article
Carro, E., Trejo, J., Gomez-Isla, T. et al. Serum insulin-like growth factor I regulates brain amyloid-β levels. Nat Med 8, 1390–1397 (2002). https://doi.org/10.1038/nm1202-793 