• Inma Castilla-Cortázar, Ignacio Iturrieta, Mariano García-Magariño, Juan E Puche, Irene Martín-Estal, Gabriel A Aguirre, Giovana Femat-Roldan, Leonel Cantu-Martinez, and Úrsula Muñoz.
• Fundacion de Investigacion HM Hospitales, Madrid, Spain; Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Ave. Morones Prieto 3000, Monterrey, N.L., Mexico, 64710. Electronic address: iccortazar@gmail.com.
• Neuroscience. 2019 Apr 15; 404: 445-458.

AbstractNeurotrophic factors (NTFs) are a relevant group of secreted proteins that modulate growth, differentiation, repair, and survival of neurons, playing a role in the maintenance of the synaptic unions, dendrites, and axons and also being crucial for peripheral nervous system development and regulating plasticity in the adult central nervous system. On the other hand, insulin-like growth factor 1 (IGF-1) has been ascertained multiple beneficial actions in the brain: neuro-development, -protection, -genesis and plasticity. To further investigate the possible mechanisms underlying IGF-1 deficiency in the establishment of neurological disease, microarray and reverse transcription polymerase chain reaction gene expression analyses coupled with in silico processing were performed in an experimental model of partial IGF-1 deficiency. Results show that the mere IGF-1 deficiency seems to be responsible for an altered expression of genes coding for neurotrophic factors (particularly ciliary neurotrophic factor and mesencephalic astrocyte-derived neurotrophic factor), their receptors and signaling pathways (specially RET). The presented findings support that IGF-1 deficiency might be involved in the establishment and progression of neurodegenerative disorders.Copyright © 2019 Elsevier Ltd. All rights reserved.

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