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High Dietary Advanced Glycation End Products Impair Mitochondrial and Cognitive Function.
Akhter, Firoz; Chen, Doris; Akhter, Asma; Sosunov, Alexander A; Chen, Allen; McKhann, Guy M; Yan, Shi Fang; Yan, Shirley ShiDu.
Afiliación
  • Akhter F; Department of Pharmacology and Toxicology and Higuchi Biosciences Center, University of Kansas, Lawrence, KS, USA.
  • Chen D; Department of Surgery, Columbia University, New York, NY, USA.
  • Akhter A; Department of Pharmacology and Toxicology and Higuchi Biosciences Center, University of Kansas, Lawrence, KS, USA.
  • Sosunov AA; Department of Pharmacology and Toxicology and Higuchi Biosciences Center, University of Kansas, Lawrence, KS, USA.
  • Chen A; Department of Surgery, Columbia University, New York, NY, USA.
  • McKhann GM; Department of Neurological Surgery and Surgery, Columbia University, New York, NY, USA.
  • Yan SF; Department of Pharmacology and Toxicology and Higuchi Biosciences Center, University of Kansas, Lawrence, KS, USA.
  • Yan SS; Department of Neurological Surgery and Surgery, Columbia University, New York, NY, USA.
J Alzheimers Dis ; 76(1): 165-178, 2020.
Article en En | MEDLINE | ID: mdl-32444539
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. OBJECTIVE: We investigated the direct effects of dietary AGEs on AGE adducts accumulation, mitochondrial function, and cognitive performance in mice. 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. 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. 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.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Productos Finales de Glicación Avanzada / Cognición / Dieta / Disfunción Cognitiva / Mitocondrias Tipo de estudio: Risk_factors_studies Límite: Animals Idioma: En Revista: J Alzheimers Dis Asunto de la revista: GERIATRIA / NEUROLOGIA Año: 2020 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Países Bajos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Productos Finales de Glicación Avanzada / Cognición / Dieta / Disfunción Cognitiva / Mitocondrias Tipo de estudio: Risk_factors_studies Límite: Animals Idioma: En Revista: J Alzheimers Dis Asunto de la revista: GERIATRIA / NEUROLOGIA Año: 2020 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Países Bajos