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Leptin gene therapy attenuates neuronal damages evoked by amyloid-beta and rescues memory deficits in APP/PS1 mice. [artículo]

Por: Antequera, Desiree [Instituto de Investigación i+12] | Carro Díaz, Eva [Instituto de Investigación i+12] | Pérez González, Rocío [Instituto de Investigación i+12].
Colaborador(es): Instituto de Investigación imas12.
Tipo de material: materialTypeLabelArtículoEditor: Gene therapy, 2014Descripción: 21(3):298-308.Recursos en línea: Solicitar documento, Resumen: There is growing evidence that leptin is able to ameliorate Alzheimer's disease (AD)-like pathologies, including brain amyloid-beta (Abeta) burden. In order to improve the therapeutic potential for AD, we generated a lentivirus vector expressing leptin protein in a self-inactivating HIV-1 vector (HIV-leptin), and delivered this by intra-cerebroventricular administration to APP/PS1 transgenic model of AD. Three months after intra-cerebroventricular administration of HIV-leptin, brain Abeta accumulation was reduced. By electron microscopy, we found that APP/PS1 mice exhibited deficits in synaptic density, which were partially rescued by HIV-leptin treatment. Synaptic deficits in APP/PS1 mice correlated with an enhancement of caspase-3 expression, and a reduction in synaptophysin levels in synaptosome preparations. Notably, HIV-leptin therapy reverted these dysfunctions. Moreover, leptin modulated neurite outgrowth in primary neuronal cultures, and rescued them from Abeta42-induced toxicity. All the above changes suggest that leptin may affect multiple aspects of the synaptic status, and correlate with behavioral improvements. Our data suggest that leptin gene delivery has a therapeutic potential for Abeta-targeted treatment of mouse model of AD.
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Artículo Artículo PC6409 (Navegar estantería) Disponible

Formato Vancouver:
Pérez-González R, Alvira-Botero MX, Robayo O, Antequera D, Garzón M, Martín-Moreno AM et al. Leptin gene therapy attenuates neuronal damages evoked by amyloid-β and rescues memory deficits in APP/PS1 mice. Gene Ther. 2014 Mar;21(3):298-308.

PMID: 24430238

Contiene 61 referencias

There is growing evidence that leptin is able to ameliorate Alzheimer's disease (AD)-like pathologies, including brain amyloid-beta (Abeta) burden. In order to improve the therapeutic potential for AD, we generated a lentivirus vector expressing leptin protein in a self-inactivating HIV-1 vector (HIV-leptin), and delivered this by intra-cerebroventricular administration to APP/PS1 transgenic model of AD. Three months after intra-cerebroventricular administration of HIV-leptin, brain Abeta accumulation was reduced. By electron microscopy, we found that APP/PS1 mice exhibited deficits in synaptic density, which were partially rescued by HIV-leptin treatment. Synaptic deficits in APP/PS1 mice correlated with an enhancement of caspase-3 expression, and a reduction in synaptophysin levels in synaptosome preparations. Notably, HIV-leptin therapy reverted these dysfunctions. Moreover, leptin modulated neurite outgrowth in primary neuronal cultures, and rescued them from Abeta42-induced toxicity. All the above changes suggest that leptin may affect multiple aspects of the synaptic status, and correlate with behavioral improvements. Our data suggest that leptin gene delivery has a therapeutic potential for Abeta-targeted treatment of mouse model of AD.

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