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Serum Insulin-like Growth Factor I in Brain Amyloid-β Levels Regulation
Posted on: December 5, 2002

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 over expressing mutant amyloid markedly reduces their brain Aβ burden, scientists consider that circulating IGF-I is a physiological regulator of brain amyloid levels with therapeutic potential.

Source: E. Carro et al. Nature Medicine December 2002 Volume 8 Number 12 pp.1390-1397
Picture: IGF-I ternary structure Pubmed; MMDB: 10220; PDB: 1BQT
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