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Circulating insulin-like growth factor I (IGF-I) enters the brain and promotes clearance of amyloid peptides known to accumulate in Alzheimer's disease (AD) brains. Both patients and mouse models of AD show decreased level of circulating IGF-I enter the brain as evidenced by a lower ratio of cerebrospinal fluid/plasma IGF-I. Importantly, in presymptomatic AD mice this reduction is already manifested as a decreased brain input of serum IGF-I in response to environmental enrichment. To explore a potential diagnostic use of this early loss of IGF-I input, we monitored electrocorticogram (ECG) responses to systemic IGF-I in mice. Whereas control mice showed enhanced ECG activity after IGF-I, presymptomatic AD mice showed blunted ECG responses. Because nonhuman primates showed identically enhanced electroencephalogram (EEG) activity in response to systemic IGF-I, loss of the EEG signature of serum IGF-I may be exploited as a disease biomarker in AD patients.This work has been supported by grants from the Spanish Ministry of Economy (Explora Program and SAF2010/17036 to IT-A and BFU2012/36107 to AN). Ángel Trueba-Sáiz holds an FPU fellowship of the Spanish Ministry of Education (ref. FPU AP2009-0372).Peer Reviewe

Loss of serum IGF-I input to the brain as an early biomarker of disease onset in Alzheimer mice