| Literature DB >> 25293421 |
Ilaria Luccarini1, Cristina Grossi1, Stefania Rigacci2, Elisabetta Coppi3, Anna Maria Pugliese1, Daniela Pantano1, Giancarlo la Marca4, Teresa Ed Dami4, Andrea Berti2, Massimo Stefani2, Fiorella Casamenti5.
Abstract
Amyloid-ß (Aß) fragments, oligomeric Aß aggregates, and pyroglutamylated-Aß peptides, as well as epigenetic mechanisms and autophagy dysfunction all appear to contribute in various ways to Alzheimer's disease progression. We previously showed that dietary supplementation of oleuropein aglycone, a natural phenol abundant in the extra virgin olive oil, can be protective by reducing Aß42 deposits in the brain of young and middle-aged TgCRND8 mice. Here, we extended our study to aged TgCRND8 mice showing increased pE3-Aß in the brain deposits. We report that oleuropein aglycone is active against glutaminylcyclase-catalyzed pE3-Aß generation reducing enzyme expression and interferes both with Aß42 and pE3-Aß aggregation. Moreover, the phenol astonishingly activates neuronal autophagy even in mice at advanced stage of pathology, where it increases histone 3 and 4 acetylation, which matches both a decrease of histone deacetylase 2 expression and a significant improvement of synaptic function. The occurrence of these functional, epigenetic, and histopathologic beneficial effects even at a late stage of the pathology suggests that the phenol could be beneficial at the therapeutic, in addition to the prevention, level.Entities:
Keywords: Alzheimer's disease; Epigenetics; Glutaminyl cyclase; Long-term potentiation; Oleuropein aglycone; Pyroglutamylated-3 Aß; TgCRND8 mice
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Year: 2014 PMID: 25293421 DOI: 10.1016/j.neurobiolaging.2014.08.029
Source DB: PubMed Journal: Neurobiol Aging ISSN: 0197-4580 Impact factor: 4.673