Gold nanoparticles crossing blood-brain barrier prevent HSV-1 infection and reduce herpes associated amyloid-βsecretion

Infections caused by HSV-1 and their typical outbreaks invading the nervous system have been related to neurodegenerative diseases. HSV-1 infection may deregulate the balance between the amyloidogenic and non-amyloidogenic pathways, raising the accumulation of amyloid-β peptides, one of the hallmark...

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Detalles Bibliográficos
Autores: Rodríguez-Izquierdo, I., Serramia, M.J., Gómez, R., de la Mata, F.J., Bullido Gómez-Heras, María Jesús, Muñoz-Fernández, M.A.
Tipo de recurso: artículo
Fecha de publicación:2020
País:España
Institución:Universidad Autónoma de Madrid
Repositorio:Biblos-e Archivo. Repositorio Institucional de la UAM
Idioma:inglés
OAI Identifier:oai:repositorio.uam.es:10486/709033
Acceso en línea:http://hdl.handle.net/10486/709033
https://dx.doi.org/10.3390/jcm9010155
Access Level:acceso abierto
Palabra clave:HSV-1
Gold nanoparticles
Central nervous system
Amyloid-β peptides
Neurodegeneration
Biología y Biomedicina / Biología
Descripción
Sumario:Infections caused by HSV-1 and their typical outbreaks invading the nervous system have been related to neurodegenerative diseases. HSV-1 infection may deregulate the balance between the amyloidogenic and non-amyloidogenic pathways, raising the accumulation of amyloid-β peptides, one of the hallmarks in the neurodegenerative diseases. An effective treatment against both, HSV-1 infections and neurodegeneration, is a major therapeutic target. Therefore, gold nanoparticles (NPAus) have been previously studied in immunotherapy, cancer and cellular disruptions with very promising results. Our study demonstrates that a new NPAus family inhibits the HSV-1 infection in a neural-derived SK-N-MC cell line model and that this new NPAus reduces the HSV-1-induced β-secretase activity, as well as amyloid-β accumulation in SK-APP-D1 modifies cell line. We demonstrated that NPAuG3-S8 crosses the blood-brain barrier (BBB) and does not generate cerebral damage to in vivo CD1 mice model. The NPAuG3-S8 could be a promising treatment against neuronal HSV-1 infections and neuronal disorders related to the Aβ peptides