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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Serum insulin-like growth factor I regulates brain amyloid-beta levels.

Levels of insulin-like growth factor I ( IGF-I), a neuroprotective hormone, decrease in serum during aging, whereas amyloid-beta ( Abeta), which is involved in the pathogenesis of Alzheimer disease, accumulates in the brain. High brain Abeta levels are found at an early age in mutant mice with low circulating IGF-I, and Abeta burden can be reduced in aging rats by increasing serum IGF-I. This opposing relationship between serum IGF-I and brain Abeta levels reflects the ability of IGF-I to induce clearance of brain Abeta, probably by enhancing transport of Abeta carrier proteins such as albumin and transthyretin into the brain. This effect is antagonized by tumor necrosis factor-alpha, a pro-inflammatory cytokine putatively involved in dementia and aging. Because IGF-I treatment of mice overexpressing mutant amyloid markedly reduces their brain Abeta burden, we consider that circulating IGF-I is a physiological regulator of brain amyloid levels with therapeutic potential.[1]

References

  1. Serum insulin-like growth factor I regulates brain amyloid-beta levels. Carro, E., Trejo, J.L., Gomez-Isla, T., LeRoith, D., Torres-Aleman, I. Nat. Med. (2002)
 
 
 
 
 
 
 
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