Estudio de las subunidades del receptor NMDA y la memoria en ratas de genotipo salvaje y transgénicas modelo de la Enfermedad de Alzheimer : desarrollo de vectores virales neurotrópicos ad hoc
NMDA receptors (NMDAR) are involved in synaptic plasticity and memory.\nThe hippocampus is involved in long term memory (LTM) formation and is affected in Alzheimer disease (AD).\nWe investigated the NMDAR regulatory subunits\nafter working memory (WM)\nand hippocampus depending LTM formation\nin ad...
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| Formato: | Tesis doctoral acceptedVersion |
| Lenguaje: | Español |
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Facultad de Farmacia y Bioquímica
2015
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| Acceso en línea: | http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgraafa&cl=CL1&d=HWA_1410 http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_1410.dir/1410.PDF |
| Aporte de: |
| Sumario: | NMDA receptors (NMDAR) are involved in synaptic plasticity and memory.\nThe hippocampus is involved in long term memory (LTM) formation and is affected in Alzheimer disease (AD).\nWe investigated the NMDAR regulatory subunits\nafter working memory (WM)\nand hippocampus depending LTM formation\nin adult young and 1 year old wild type (Controls) and\ntransgenic rats (Tg)\n(McGill-?R-?Thy1-?APP), modeling AD.\nAll of them showed WM and LTM, but the transient increases in GluN1 and GluN2A detected in young\nrats following habituation, did not take place in older rats, suggesting that this mechanism is impaired and\nthat the change would not be required to form a LTM.\nTo evaluate the involvement of those subunits in memory, we developed amplicon vectors to express antisense RNA (AS) against GluN2A and\nGluN2B.\nRats injected with 2A(AS)\nvectors into the hippocampus, expressed both WM and LTM.\nThose injected with 2B(AS)\nshowed impaired and delayed WM, without LTM\nexpression.\nTherefore, GluN2B, to which oligomers of the amyloid beta peptide (o?A)\nbind in early AD, would not\nbe an acceptable therapeutic target.\nThen, we developed a single chain antibody against oA?,a plasmid to express it in eukaryotic cells, to produce amplicon vectors as a feasible experimental therapy against AD. |
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