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Intranasal neprilysin rapidly eliminates amyloid-beta plaques, but causes plaque compensations: the explanation why the amyloid-beta cascade may fail?
Neurodegenerative brain disorders are a major burden in our society, such as Alzheimer´s disease. In order to repair or prevent such diseases, drugs are designed which enter the brain, but the blood-brain barrier limits their entry and the search for alternative pathways is important. Recently, we r...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Wolters Kluwer - Medknow
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8848595/ https://www.ncbi.nlm.nih.gov/pubmed/35142662 http://dx.doi.org/10.4103/1673-5374.335138 |
Sumario: | Neurodegenerative brain disorders are a major burden in our society, such as Alzheimer´s disease. In order to repair or prevent such diseases, drugs are designed which enter the brain, but the blood-brain barrier limits their entry and the search for alternative pathways is important. Recently, we reported that intranasal delivery of the amyloid-beta degrading enzyme neprilysin eliminated amyloid-beta plaques in transgenic Alzheimer´s disease mice. This review describes the anatomical structure of the intranasal pathway, explains the intranasal delivery of pure neprilysin, cell-loaded neprilysin (platelets) and collagen-embedded neprilysin to destruct amyloid-beta plaques in Alzheimer´s disease in transgenic APP_SweDI mice and hypothesizes why this may cause compensation and why the amyloid-beta cascade hypothesis may fail. |
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