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High dietary advanced glycation end products are associated with poorer spatial learning and accelerated Aβ deposition in an Alzheimer mouse model
I. Lubitz, J. Ricny, D. Atrakchi-Baranes, C. Shemesh, E. Kravitz, S. Liraz-Zaltsman, A. Maksin-Matveev, I. Cooper, A. Leibowitz, J. Uribarri, J. Schmeidler, W. Cai, Z. Kristofikova, D. Ripova, D. LeRoith, M. Schnaider-Beeri,
Jazyk angličtina Země Anglie, Velká Británie
Typ dokumentu časopisecké články, práce podpořená grantem
Free Medical Journals od 2002 do Před 2 roky
PubMed Central od 2008
ProQuest Central od 2014-02-01 do 2017-12-31
Open Access Digital Library od 2002-01-01
Open Access Digital Library od 2011-01-01
Open Access Digital Library od 2014-01-01
Medline Complete (EBSCOhost) od 2003-02-01
Wiley-Blackwell Open Access Titles od 2002
ROAD: Directory of Open Access Scholarly Resources od 2002
Odkazy
PubMed
26781037
DOI
10.1111/acel.12436
Knihovny.cz E-zdroje
- MeSH
- Alzheimerova nemoc metabolismus MeSH
- amyloidní beta-protein metabolismus MeSH
- dieta MeSH
- modely nemocí na zvířatech MeSH
- myši inbrední C57BL MeSH
- myši MeSH
- náhodné rozdělení MeSH
- produkty pokročilé glykace aplikace a dávkování metabolismus MeSH
- prostorové učení fyziologie MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
There is growing evidence of the involvement of advanced glycation end products (AGEs) in the pathogenesis of neurodegenerative processes including Alzheimer's disease (AD) and their function as a seed for the aggregation of Aβ, a hallmark feature of AD. AGEs are formed endogenously and exogenously during heating and irradiation of foods. We here examined the effect of a diet high in AGEs in the context of an irradiated diet on memory, insoluble Aβ42 , AGEs levels in hippocampus, on expression of the receptor for AGEs (RAGE), and on oxidative stress in the vasculature. We found that AD-like model mice on high-AGE diet due to irradiation had significantly poorer memory, higher hippocampal levels of insoluble Aβ42 and AGEs as well as higher levels of oxidative stress on vascular walls, compared to littermates fed an isocaloric diet. These differences were not due to weight gain. The data were further supported by the overexpression of RAGE, which binds to Aβ42 and regulates its transport across the blood-brain barrier, suggesting a mediating pathway. Because exposure to AGEs can be diminished, these insights provide an important simple noninvasive potential therapeutic strategy for alleviating a major lifestyle-linked disease epidemic.
Department of Internal Medicine D and Hypertension Unit Sheba Medical Center Ramat Gan 52621 Israel
Department of Medicine Icahn School of Medicine at Mt Sinai New York NY 10029 USA
Department of Psychiatry Mount Sinai School of Medicine New York NY 10029 USA
The Joseph Sagol Neuroscience Center Tel Hashomer Ramat Gan 52621 Israel
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