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High Dietary Advanced Glycation End Products Impair Mitochondrial and Cognitive Function.
- Source :
-
Journal of Alzheimer's disease : JAD [J Alzheimers Dis] 2020; Vol. 76 (1), pp. 165-178. - Publication Year :
- 2020
-
Abstract
- Background: Advanced glycation end products (AGEs) are an important risk factor for the development of cognitive decline in aging and late-onset neurodegenerative diseases including Alzheimer's disease. However, whether and how dietary AGEs exacerbate cognitive impairment and brain mitochondrial dysfunction in the aging process remains largely unknown.<br />Objective: We investigated the direct effects of dietary AGEs on AGE adducts accumulation, mitochondrial function, and cognitive performance in mice.<br />Methods: Mice were fed the AGE+ diet or AGE- diet. We examined levels of AGE adducts in serum and cerebral cortexes by immunodetection and immunohistochemistry, determined levels of reactive oxygen species by biochemical analysis, detected enzyme activity associated with mitochondrial respiratory chain complexes I & IV and ATP levels, and assessed learning and memory ability by Morris Water Maze and nesting behavior.<br />Results: Levels of AGE adducts (MG-H1 and CEL) were robustly increased in the serum and brain of AGE+ diet fed mice compared to the AGE- group. Furthermore, greatly elevated levels of reactive oxygen species, decreased activities of mitochondrial respiratory chain complexes I & IV, reduced ATP levels, and impaired learning and memory were evident in AGE+ diet fed mice compared to the AGE- group.<br />Conclusion: These results indicate that dietary AGEs are important sources of AGE accumulation in vivo, resulting in mitochondrial dysfunction, impairment of energy metabolism, and subsequent cognitive impairment. Thus, reducing AGEs intake to lower accumulation of AGEs could hold therapeutic potential for the prevention and treatment of AGEs-induced mitochondrial dysfunction linked to cognitive decline.
- Subjects :
- Animals
Cognition drug effects
Energy Metabolism drug effects
Energy Metabolism physiology
Female
Glycation End Products, Advanced administration & dosage
Male
Maze Learning drug effects
Maze Learning physiology
Mice
Mice, Inbred C57BL
Mitochondria drug effects
Reactive Oxygen Species metabolism
Cognition physiology
Cognitive Dysfunction chemically induced
Cognitive Dysfunction metabolism
Diet adverse effects
Glycation End Products, Advanced toxicity
Mitochondria metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1875-8908
- Volume :
- 76
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Journal of Alzheimer's disease : JAD
- Publication Type :
- Academic Journal
- Accession number :
- 32444539
- Full Text :
- https://doi.org/10.3233/JAD-191236