High dietary advanced glycation end products are associated with poorer spatial learning and accelerated Aβ deposition in an Alzheimer mouse model
| Autor: | Derek LeRoith, Dana Atrakchi-Baranes, Michal Schnaider-Beeri, Jaime Uribarri, Anna Maksin‐Matveev, Weijing Cai, Avshalom Leibowitz, James Schmeidler, Irit Lubitz, Jan Ricny, Itzik Cooper, Sigal Liraz-Zaltsman, Efrat Kravitz, Zdena Kristofikova, Chen Shemesh, Daniela Ripova |
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| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Glycation End Products Advanced Male Aging medicine.medical_specialty Spatial Learning Hippocampus Context (language use) Biology Bioinformatics Blood–brain barrier medicine.disease_cause blood–brain barrier advanced glycation end product RAGE (receptor) Tg2576 Pathogenesis 03 medical and health sciences chemistry.chemical_compound Mice Random Allocation 0302 clinical medicine Glycation Alzheimer Disease Internal medicine receptor for advanced glycation end product medicine Animals Aβ Amyloid beta-Peptides Cell Biology Original Articles Alzheimer's disease Diet Mice Inbred C57BL Disease Models Animal 030104 developmental biology Endocrinology medicine.anatomical_structure chemistry Advanced glycation end-product Original Article Female 030217 neurology & neurosurgery Oxidative stress |
| Zdroj: | Aging Cell |
| ISSN: | 1474-9726 1474-9718 |
| Popis: | Summary 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. |
| Databáze: | OpenAIRE |
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