IGF1 gene therapy delays reproductive senescence.

FALOMIR LOCKHART E; GARCIA-SEGURA LM; HERRERA M.; AREVALO MA.; DOLCETTI FRANCO; HEREÑÚ C.; BELLINI MJ

Córdoba Capital

Congreso; SAN 2018; 2018

Sociedad Argentina de Neurociencias

INTRODUCTIONAgingis characterized by a coordinated organs and tissues functionalimpairment The hypothalamus, a region known to regulate many basicfunctions such as growth, development, reproduction and metabolism, isproposed as a regulatory center of aging Evidence demonstrates that theinhibition or activation of microglial or neural transcription factor NF κB of thebasal hypothalamus ( affects the life expectancy and the " ofaging, as well as the release of GnRH There is solid evidence that middle age( rats do not respond to estradiol positive feedback with an appropriatemodulation of excitatory and inhibitory hypothalamic neurotransmitter releaseThis imbalance could cause reduced activation of GnRH neurons, reduced GnRHrelease, and an abnormal LH surge The MA rat brain reduction of factors likeIGF 1 could be the reason of the affected modulation on excitatory andinhibitory hypothalamic release These findings provide a link betweeninflammation, response to stress and systemic and cerebral agingHYPOTHESIS It is well known that IGF 1 plays a physiological role in neuroprotection andneuroinflammation We decided to investigate the effects of intrahypothalamicIGF 1 gene therapy in MA rats We propose that transgenic IGF 1 will modulateneuroinflammation and delay reproductive senescenceCONCLUSIONSOurs results suggest that IGF 1 prolongs the reproductive life ofMA rats, maintaining GnRH neurons functionality, this could bemediated by kisspeptin positive feedback