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http://hdl.handle.net/2445/155477
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DC Field | Value | Language |
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dc.contributor.author | Tavares, Eva | - |
dc.contributor.author | Antequera, Desiree | - |
dc.contributor.author | López González, Irene | - |
dc.contributor.author | Ferrer, Isidro (Ferrer Abizanda) | - |
dc.contributor.author | Miñano, Francisco J. | - |
dc.contributor.author | Carro, Eva | - |
dc.date.accessioned | 2020-04-16T09:04:17Z | - |
dc.date.available | 2020-04-16T09:04:17Z | - |
dc.date.issued | 2016-10-01 | - |
dc.identifier.issn | 0002-9440 | - |
dc.identifier.uri | http://hdl.handle.net/2445/155477 | - |
dc.description.abstract | Increasing evidence suggests that inflammatory responses cause brain atrophy and play a prominent and early role in the progression of Alzheimer disease. Recent findings show that the neuroendocrine peptide aminoprocalcitonin (NPCT) plays a critical role in the development of systemic inflammatory response; however, the presence, possible function, regulation, and mechanisms by which NPCT may be involved in Alzheimer disease neuropathology remain unknown. We explored the expression of NPCT and its interaction with amyloid-b (Ab), and proinflammatory and neurogenic effects. By using brain samples of Alzheimer disease patients and APP/PS1 transgenic mice, we evaluated the potential role of NPCT on Ab-related pathology. We found that NPCT is expressed in hippocampal and cortical neurons and Ab-induced up-regulation of NPCT expression. Peripherally administered antibodies against NPCT decreased microglial activation, decreased circulating levels of proinflammatory cytokines, and prevented Ab-induced neurotoxicity in experimental models of Alzheimer disease. Remarkably, anti-NPTC therapy resulted in a significant improvement in the behavioral status of APP/PS1 mice. Our results indicate a central role of NPCT in Alzheimer disease pathogenesis and suggest NPCT as a potential biomarker and therapeutic target. | - |
dc.format.extent | 13 p. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Elsevier | - |
dc.relation.isformatof | Versió postprint del document publicat a: https://doi.org/10.1016/j.ajpath.2016.06.006 | - |
dc.relation.ispartof | American Journal of Pathology, 2016, vol. 186, num. 10, p. 2723-2735 | - |
dc.relation.uri | https://doi.org/10.1016/j.ajpath.2016.06.006 | - |
dc.rights | cc-by-nc-nd (c) American Society for Investigative Pathology, 2016 | - |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/3.0/es | - |
dc.source | Articles publicats en revistes (Patologia i Terapèutica Experimental) | - |
dc.subject.classification | Malaltia d'Alzheimer | - |
dc.subject.classification | Etiologia | - |
dc.subject.classification | Calcitonina | - |
dc.subject.classification | Metabolisme | - |
dc.subject.other | Alzheimer's disease | - |
dc.subject.other | Etiology | - |
dc.subject.other | Calcitonin | - |
dc.subject.other | Metabolism | - |
dc.title | Potential role of aminoprocalcitonin in the pathogenesis of alzheimer disease | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/acceptedVersion | - |
dc.identifier.idgrec | 667197 | - |
dc.date.updated | 2020-04-16T09:04:17Z | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
dc.identifier.pmid | 27497681 | - |
Appears in Collections: | Articles publicats en revistes (Patologia i Terapèutica Experimental) Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) |
Files in This Item:
File | Description | Size | Format | |
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667197.pdf | 2.59 MB | Adobe PDF | View/Open |
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