Beta-Amyloid monomer and insulin/IGF-1 signaling in Alzheimer's disease

Maria Laura Giuffrida, Flora Tomasello, Filippo Caraci, Santina Chiechio, Ferdinando Nicoletti, Agata Copani

Research output: Contribution to journalArticlepeer-review


Alzheimer's disease is the most common form of dementia among older people and is still untreatable. While β-amyloid protein is recognized as the disease determinant with a pivotal role in inducing neuronal loss and dementia, an impaired brain insulin signaling seems to account in part for the cognitive deficit associated with the disease. The origin of this defective signaling is uncertain. Accumulating toxic species of β-amyloid, the so-called oligomers, has been proposed to be responsible for downregulation of neuronal insulin receptors. We have found that the nontoxic form of β-amyloid, the monomer, is able to activate insulin/insulin-like growth factor-1 (IGF-1) receptor signaling and thus behaves as a neuroprotectant agent. Our suggestion is that depletion of β-amyloid monomers, occurring in the preclinical phase of Alzheimer's disease, might be the cause of early insulin/IGF-1 signaling disturbances that anticipate cognitive decline.

Original languageEnglish
Pages (from-to)605-613
Number of pages9
JournalMolecular Neurobiology
Issue number3
Publication statusPublished - 2012


  • β-Amyloid
  • Alzheimer's disease
  • Insulin
  • Insulin-like growth factor 1

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience


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