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Título

The role of insulin and insulin-like growth factor I in the molecular and cellular mechanisms underlying the pathology of Alzheimer's disease

AutorCarro, E.; Torres Alemán, Ignacio
Palabras claveAlzheimer's disease Insulin Insulin-like growth factor I β Amyloid Blood–brain barrier Tau
Fecha de publicación2004
EditorElsevier
CitaciónEuropean Journal of Pharmaceutics and Biopharmaceutics 490: 127- 133 (2004)
ResumenCellular and molecular processes leading to abnormal accumulation of β amyloid in the brain are slowly being uncovered. A potential involvement of insulin and insulin-like growth factor I (IGF-I) in this plausible pathogenic process in Alzheimer's disease has recently been proposed. Evidence favoring this idea stems from the ability of both hormones to stimulate β amyloid release from neurons as well as by the stimulatory effect that IGF-I exerts on brain amyloid clearance. In addition, insulin and IGF-I levels are altered in Alzheimer's patients and, probably in close association to these changes, cell sensitivity towards insulin - and possibly also IGF-I - is decreased in these patients. We now review evidence that disturbed insulin/IGF-I signaling to brain cells, initiated at the level of the blood-brain barriers is probably instrumental in development of brain amyloidosis. Furthermore, insulin and IGF-I are potent neuroprotective factors and can regulate levels of phosphorylated tau, a major component of neurofibrillary tangles found in Alzheimer's brains. Therefore, a decrease in trophic support to neurons together with increased tau phosphorylation will follow loss of sensitivity towards insulin and IGF-I. Altogether, this supports the notion that a single pathogenic event, i.e., brain resistance to insulin/IGF-I, accounts for neuronal atrophy/death, tangle formation and brain amyloidosis typical of Alzheimer's pathology. © 2004 Elsevier B.V. All rights reserved.
URIhttp://hdl.handle.net/10261/153713
DOI10.1016/j.ejphar.2004.02.050
Identificadoresdoi: 10.1016/j.ejphar.2004.02.050
issn: 0014-2999
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