Publicación:
Serum Insulin-Like Growth Factor I Deficiency Associates to Alzheimer's Disease Co-Morbidities
Serum Insulin-Like Growth Factor I Deficiency Associates to Alzheimer's Disease Co-Morbidities
| dc.contributor.author | Zegarra-Valdivia, JA | es_PE |
| dc.contributor.author | Santi, A | es_PE |
| dc.contributor.author | de Sevilla, MEF | es_PE |
| dc.contributor.author | Nunez, A | es_PE |
| dc.contributor.author | Aleman, IT | es_PE |
| dc.date.accessioned | 2024-05-30T23:13:38Z | |
| dc.date.available | 2024-05-30T23:13:38Z | |
| dc.date.issued | 2019 | |
| dc.description | We are thankful to M. Garcia for technical support. This work was funded by a grant from Ciberned, by and Inter-CIBER project (PIE14/00061), and from SAF2016-76462-C2-1-P (MINECO). J.A. ZegarraValdivia acknowledges the financial support from the National Council of Science, Technology and Technological Innovation (CONCYTEC, Peru) through ´the National Fund for Scientific and Technological Development (FONDECYT, Peru). ´Authors’ disclosures available online (https://www.j-alz.com/manuscript-disclosures/19-0241). | |
| dc.description.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. | |
| dc.description.sponsorship | Consejo Nacional de Ciencia, Tecnología e Innovación Tecnológica - Concytec | |
| dc.identifier.doi | https://doi.org/10.3233/JAD-190241 | |
| dc.identifier.isi | 472086100008 | |
| dc.identifier.uri | https://hdl.handle.net/20.500.12390/1142 | |
| dc.language.iso | eng | |
| dc.publisher | IOS Press, Inc. | |
| dc.relation.ispartof | Journal of Alzheimer's Disease | |
| dc.rights | info:eu-repo/semantics/openAccess | |
| dc.subject | insulin-like growth factor 1 | |
| dc.subject | Alzheimer’s disease | es_PE |
| dc.subject | animal models of disease | es_PE |
| dc.subject | co-morbidities | es_PE |
| dc.subject.ocde | https://purl.org/pe-repo/ocde/ford#3.02.00 | |
| dc.title | Serum Insulin-Like Growth Factor I Deficiency Associates to Alzheimer's Disease Co-Morbidities | |
| dc.type | info:eu-repo/semantics/article | |
| dspace.entity.type | Publication | |
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