Affiliations: [a]
Cajal Institute (CSIC), Madrid, Spain
| [b] Universidad Nacional de San Agustín de Arequipa, Perú | [c] CIBERNED, Spain
| [d] Department of Neurosciences, School of Medicine, UAM, Madrid, Spain
Correspondence:
[*]
Correspondence to: Ignacio Torres Aleman, Cajal Institute, CSIC, Avda Dr Arce 37, 28002 Madrid, Spain. Tel.: +34 915854723; Fax: +34 915854754; E-mail: torres@cajal.csic.es.
Abstract: Increasing evidence supports the notion that Alzheimer’s disease (AD), a condition that presents heterogeneous pathological disturbances, is also associated to perturbed metabolic function affecting insulin and insulin-like growth factor I (IGF-I). While impaired insulin activity leading to insulin resistance has been associated to AD, whether altered IGF-I function affects the disease is not entirely clear. Despite the limitations of mouse models to mimic AD pathology, we took advantage that serum IGF-I deficient mice (LID mice) present many functional perturbations present in AD, most prominently cognitive loss, which is reversed by treatment with systemic IGF-I. We analyzed whether these mice display other pathological traits that are usual co-morbidities of AD. We found that LID mice not only display cognitive disturbances, but also show altered mood and sociability, increased susceptibility to epileptiform activity, and a disturbed sleep/wake cycle. Collectively, these data suggest that reduced IGF-I activity contributes to heterogeneous deficits commonly associated to AD. We suggest that impaired IGF-I activity needs to be taken into consideration when modeling this condition.
