Herrera Macarena L1, Espejo Pablo J1,Deza-Ponzio Romina1, Calfa Gastón D1,Bellini María José2, Molina Victor A*1and Hereñú Claudia B*1. *equally contribution. EarlyCognitive Impairment associated with a parkinsonian animal model: synapticplasticity and initial approaches with IGF-1 gene therapy. Sociedad Argentinade Neurociencias, SAN, 25-27 Sept. 2017. Mar del Plata, Buenos Aires, Argentina.
Abstract: Early CognitiveImpairment associated with a parkinsonian animal model: synaptic plasticity andinitial approaches with IGF-1 gene therapy.
Herrera Macarena L1, Espejo Pablo J1, Deza-PonzioRomina1, Calfa Gastón D1,Bellini María José2, MolinaVictor A*1and HereñúClaudia B*1 *equally contribution
1Institutode Farmacología Experimental de Córdoba (IFEC)- Depto.Farmacología-FCQ-UNC-CONICET-Córdoba, Córdoba, Argentina.
2Institutode Investigaciones Bioquímicas de La Plata (INIBIOLP)- FCM-UNLP-CONICET-La Plata,Buenos Aires, Argentina.
Abstract: Parkinson´s disease(PD) is a neurodegenerative disorder with a progressive dopaminergic (DA)neuronal loss and a variety of non-motor symptoms such as cognitivedysfunctions Growth factors as IGF-1 could be neuroprotective in PD models byimprove changes in neuronal activity. 1) To determine the early cognitivedecline and the correlation of hippocampal changes in 6OHDA model 2) to carryout therapeutic approaches with IGF-1 to understand plasticity processes associatedwith cognitive decline. Male Wistar rats were CPu bilaterally injected with6OHDA or vehicle (SHAM). Independent groups were tested after 7, 14, 20 and 28days for Y-maze and locomotor activity. Another set of rats were divided into 6groups according the adenoviral therapy in hippocampus: SHAM, 6OHDA, SHAM-RAd-DS-Red, SHAM-RAd-IGF-1,6OHDA-RAd-DS-Red and 6OHDA-RAd-IGF-1. At 20 days post lesion, were tested forbehavioral tasks. Then rats were perfused, the brains fixed and IHQ performedfor TH and IGF-1R and hippocampal synaptic plasticity. At 20 post-lesion,memory deficits, changes in dendritic spines were observed in 6OHDA ratscompared to SHAM rats. This behavioral cognitive decline was partially modifiedwith IGF-1 overexpression in 6OHDA-RAd-IGF-1 rats. 6-OHDA was sufficient tocause memory impairments. Knowledge of this neurodegenerative progression couldresult in potential therapeutic strategies as IGF-1 gene therapy whichmotivates us to further studies under this experimental model.
