Dietary advanced glycation end products are associated with decline in memory in young elderly

West, Rebecca; Moshier, Erin; Lubitz, Irit; Schmeidler, James; Godbold, James; Cai, Weiping; Uribarri, Jaime; Vlassara, Helen; Silverman, Jeremy M.; Beeri, Michal Schnaider

doi:10.1016/j.mad.2014.07.001

Cited by 75 publications

(54 citation statements)

References 17 publications

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“…In continuation of this outcome, the animal model of accelerated ageing (enhanced glycation) was developed (using high fructose diet) to assess the effect of GLA in vivo. Literature revealed that fructose accelerates glycation and production of AGEs (Farooqui 2013), which subsequently cause memory impairment (Yaffe et al 2011;West et al 2014). Our data also showed impairment in spatial learning of fructosetreated animals during acquisition phase (Figure 2(b)) as Figure 5.…”

Section: Discussionsupporting

confidence: 71%

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Gamma-linolenic acid ameliorated glycation-induced memory impairment in rats

Khan

Haider

Mahmood

et al. 2017

Pharmaceutical Biology

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Objective: The current study investigates the anti-ageing effect of GLA in Sprague-Dawley rats. Materials and methods: GLA (0.1, 0.2, 0.4, 2, 10, 20 and 24 lM) was initially evaluated for its effect on the formation of advanced glycation end products (AGEs) in vitro. For in vivo assessment (1, 5 or 15 mg/ kg), the rat model of accelerated ageing was developed using D-fructose (1000 mg/kg (i.p.) plus 10% in drinking water for 40 days). Morris water maze was used to evaluate impairment in learning and memory. The blood of treated animals was used to measure glycosylated haemoglobin (HbA1c) levels. The interaction of GLA with active residues of receptor of AGE (RAGE) was analyzed using AutoDock Vina. Results: Our data showed that GLA inhibited the production of AGEs (IC 50 ¼ 1.12 ± 0.05 lM). However, this effect was more significant at lower tested doses. A similar pattern was also observed in in vivo experiments, where the effect of fructose was reversed by GLA only at lowest tested dose of 1 mg/kg. The HbA1c levels also revealed significant reduction at lower doses (1 and 5 mg/kg). The in silico data exhibited promising interaction of GLA with active residues (Try72, Arg77 and Gln67) of RAGE. Conclusion: The GLA, at lower doses, possesses therapeutic potential against glycation-induced memory decline. ARTICLE HISTORY

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Section: Discussionsupporting

confidence: 71%

“…In this regard, fructose is reported to enhance the production of AGEs (Farooqui 2013) and presumably memory impairment in humans (Yaffe et al 2011;West et al 2014). In animals, the large doses of fructose have also been reported to escalate the glycation, thereby leading to the development of associated anomalies (Rodriguez et al 1994).…”

Section: Introductionmentioning

confidence: 99%

Gamma-linolenic acid ameliorated glycation-induced memory impairment in rats

Khan

Haider

Mahmood

et al. 2017

Pharmaceutical Biology

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“…However, the cause for this aggregation is still unclear. Although accumulation of AGEs is a normal feature of aging (Luth et al ., 2005), in AD, it is accelerated (West et al ., 2014). AGEs modification may explain many of the neuropathological and biochemical features of AD such as extensive protein cross‐linking, oxidative stress, and neuronal cell death.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, there is evidence of AGEs involvement in the pathogenesis of neurodegenerative processes including Alzheimer's disease (AD) (Grossman, 2003). We recently reported that elevated serum AGEs level is associated with a faster rate of cognitive decline (Beeri et al ., 2011; West et al ., 2014). …”

Section: Introductionmentioning

confidence: 99%

High dietary advanced glycation end products are associated with poorer spatial learning and accelerated Aβ deposition in an Alzheimer mouse model

et al. 2016

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SummaryThere 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.

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“…Por outro lado, o elevado consumo de dieta rica em AGE associa-se com perda de capacidade cognitiva e memória em idosos (West et al, 2014). (2004) demonstraram que a LDL modificada por AGE, isolada de portadores de diabete melito que ingeriram dieta rica em AGE, aumenta as vias de sinalização intracelular associadas à produção de marcadores inflamatórios.…”

Section: Produtos De Glicação Avançadaunclassified

Aterogênese induzida por albumina modificada por glicação avançada em camundongos dislipidêmicos é previnida pelo tratamento com losartana

Gomes¹

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duas das mais divertidas técnicas de laboratório, por toda a ajuda no decorrer desse projeto, por me ajudarem a encontrar equipamentos, solventes, reagentes e outros materiais, por ouvirem meus desabafos e cantorias, por sempre apoiarem às nossas celebrações de meio de ano, além de sempre me divertirem, permitindo com que eu fizesse comentários engraçados durante uma conversa séria, sem se magoarem.À Claudia Souza, Clau, que por muitas vezes parou o que estava fazendo para me ajudar com alguma burocracia administrativa, agradeço pela responsabilidade com que levastes a administração desse projeto, pelas conversas, cafés e brincadeiras.À Jussara Rocha, Ju, por ter me ensinado o mais básico de tudo sobre o laboratório e suas técnicas, sempre de maneira solícita e com um sorriso no rosto.À Rosibel Silva, pelas conversas, pelo cafezinho e pela organização das salas; e à dona Ana, por deixar tudo sempre limpo para que pudéssemos trabalhar.À Senária Eguti, Se, e a Maria Aparecida da Silva, Cida, secretárias da pós-graduação que nunca deixaram de me ajudar, desde às exigências do Programa, até à candidatura para bolsas de estudos.Aos doutores Mônica Neves e Ísio Schultz pelas contribuições em nossas reuniões científicas semanais.Àqueles que tiveram uma passagem breve pelo laboratório: Karina Oliveira, por conversas superengraçadas que fizeram as tardes passar bem rápido; Eliton Juniro da Silva, por me ajudar com os protocolos e sempre demonstrar interesse sobre a minha pesquisa, discutindo e perguntando, além de se tornar confidente sobre os problemas que somente nós entenderíamos.Simone Batista e Bruna Lacerda, por contribuírem para que os dias fossem melhores e sempre tivéssemos um assunto diferente para conversar.À nova geração dessa família LIM10, Lis Mie, Guilherme Ferreira, Ana Paula Lembo, e Vanessa Del Bianco, que já participam com muita vontade da rotina do laboratório e nos ajudam a relembrar conceitos básicos do que aprendemos. Muito sucesso nesse caminho. Às doutoras Walcy Paganelli Rosolia Teodoro, responsável pelo Laboratório de Matriz Extracelular da Disciplina de Reumatologia, e Ana PaulaVelosa, por acreditarem neste projeto e aceitarem participar do desenvolvimento do mesmo. Dra Walcy, agradeço-a por todas as longas tardes em seu laboratório regadas a muito bom humor, conversas, um antigo rádio tocando músicas dos anos 80 e por sempre me tratar como membro do seu grupo.Às alunas Isabelle Camargo e Verônica Protocevich, membros do laboratório da Dra. Walcy, por me ajudarem nas análises histomorfométricas e de imunofluorencência.Aos egressos do nosso grupo que contribuíram de maneira importante à minha trajetória: doutor Raphael Souza Pinto, por toda ajuda de bancada; doutora Débora Rocco, por me ajudar a entender, logo que entrei para o laboratório, muito do que havia sido discutido nas reuniões científicas; doutora Roberta Marcondes Machado, por "velejar" comigo em discussões de artigos, sempre com bom humor; doutora Renata Bombo, pelas conversas, brincadeiras e dicas de viagens; e doutora Camila Cante...

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Dietary advanced glycation end products are associated with decline in memory in young elderly

Cited by 75 publications

References 17 publications

Gamma-linolenic acid ameliorated glycation-induced memory impairment in rats

Gamma-linolenic acid ameliorated glycation-induced memory impairment in rats

High dietary advanced glycation end products are associated with poorer spatial learning and accelerated Aβ deposition in an Alzheimer mouse model

Aterogênese induzida por albumina modificada por glicação avançada em camundongos dislipidêmicos é previnida pelo tratamento com losartana

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