{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T00:21:10Z","timestamp":1788481270323,"version":"build-2803163510"},"reference-count":41,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2017,8,12]],"date-time":"2017-08-12T00:00:00Z","timestamp":1502496000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100006087","name":"Direcci\u00f3n General de Asuntos del Personal Acad\u00e9mico, Universidad Nacional Aut\u00f3noma de M\u00e9xico","doi-asserted-by":"publisher","award":["209212"],"award-info":[{"award-number":["209212"]}],"id":[{"id":"10.13039\/501100006087","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100006087","name":"Direcci\u00f3n General de Asuntos del Personal Acad\u00e9mico, Universidad Nacional Aut\u00f3noma de M\u00e9xico","doi-asserted-by":"publisher","award":["G. P\u2010A 209513"],"award-info":[{"award-number":["G. P\u2010A 209513"]}],"id":[{"id":"10.13039\/501100006087","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2018,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>\u03b2\u2010Amyloid peptide accumulation in the cortex and in the hippocampus results in neurodegeneration and memory loss. Recently, it became evident that the inflammatory response triggered by \u03b2\u2010Amyloid peptides promotes neuronal cell death and degeneration. In addition to inflammation, \u03b2\u2010Amyloid peptides also induce alterations in neuronal autophagy, eventually leading to neuronal cell death. Thus, here we evaluated whether the inflammatory response induced by the \u03b2\u2010Amyloid peptides impairs memory via disrupting the autophagic flux. We show that male mice overexpressing \u03b2\u2010Amyloid peptides (5XFAD) but lacking caspase\u20101, presented reduced \u03b2\u2010Amyloid plaques in the cortex and in the hippocampus; restored brain autophagic flux and improved learning and memory capacity. At the molecular level, inhibition of the inflammatory response in the 5XFAD mice restored LC3\u2010II levels and prevented the accumulation of oligomeric p62 and ubiquitylated proteins. Furthermore, caspase\u20101 deficiency reinstates activation of the AMPK\/Raptor pathway while down\u2010regulating AKT\/mTOR pathway. Consistent with this, we found an inverse correlation between the increase of autophagolysosomes in the cortex of 5XFAD mice lacking caspase\u20101 and the presence of mitochondria with altered morphology. Together our results indicate that \u03b2\u2010Amyloid peptide\u2010induced caspase\u20101 activation, disrupts autophagy in the cortex and in the hippocampus resulting in neurodegeneration and memory loss.<\/jats:p>","DOI":"10.1002\/jnr.24130","type":"journal-article","created":{"date-parts":[[2017,8,12]],"date-time":"2017-08-12T08:16:37Z","timestamp":1502525797000},"page":"234-246","source":"Crossref","is-referenced-by-count":35,"title":["Autophagy impairment by caspase\u20101\u2010dependent inflammation mediates memory loss in response to \u03b2\u2010Amyloid peptide accumulation"],"prefix":"10.1002","volume":"96","author":[{"given":"Lourdes","family":"\u00c1lvarez\u2010Arellano","sequence":"first","affiliation":[{"name":"Laboratorio de Neuroinmunobiolog\u00eda, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnolog\u00eda, Universidad Nacional Aut\u00f3noma de M\u00e9xico Cuernavaca Mor. 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