Serum Insulin-Like Growth Factor I Deficiency Associates to Alzheimer’s Disease Co-Morbidities
| Autor: | Ignacio Torres Aleman, Jonathan A. Zegarra-Valdivia, Maria Estrella Fernandez de Sevilla, Angel Nuñez, Andrea Santi |
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| Přispěvatelé: | Ministerio de Economía y Competitividad (España), Consejo Nacional de Ciencia, Tecnología e Innovación Tecnológica (Perú), Fondo Nacional de Desarrollo Científico, Tecnológico y de Información Tecnológica (Perú) |
| Rok vydání: | 2019 |
| Předmět: |
Male
0301 basic medicine Insulin-like growth factor 1 medicine.medical_specialty medicine.medical_treatment Disease Mice 03 medical and health sciences 0302 clinical medicine Insulin resistance Alzheimer Disease Internal medicine Animal models of disease Animals Humans Medicine Co-morbidities Insulin-Like Growth Factor I Maze Learning Social Behavior Pathological Mood Disorders business.industry General Neuroscience Growth factor Insulin Cognition General Medicine medicine.disease Mice Inbred C57BL Disease Models Animal Psychiatry and Mental health Clinical Psychology 030104 developmental biology Mood Endocrinology Female Co morbidity Geriatrics and Gerontology Cognition Disorders business Alzheimer’s disease 030217 neurology & neurosurgery |
| Zdroj: | Digital.CSIC. Repositorio Institucional del CSIC instname |
| ISSN: | 1875-8908 1387-2877 |
| Popis: | 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. We are thankful to M. García 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. Zegarra-Valdivia acknowledges the financial support from the National Council of Science, Technology and Technological Innovation (CONCYTEC, Perú) through the National Fund for Scientific and Technological Development (FONDECYT, Perú). |
| Databáze: | OpenAIRE |
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