Observational and Ecological Studies of Dietary Advanced Glycation End Products in National Diets and Alzheimer's Disease Incidence and Prevalence

Perrone, Lorena; Grant, William B.

doi:10.3233/jad-140720

Cited by 63 publications

(52 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Evidence from human and animal levels support that long‐term dAGEs intake might adversely affect cognitive function (Cai et al, ; Lubitz et al, ; Perrone & Grant, ). Our study is the very first to demonstrate that even a 21 days of diet rich in dAGEs was capable of inducing cognitive impairment in aged ICR mice.…”

Section: Discussionmentioning

confidence: 99%

“…The cardinal hallmarks of AD mainly include amyloid beta senile plaques and neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau in the brain (Lane, Hardy, & Schott, ). Until now, the exact causal factors of AD remain not completely explored, while existing evidence suggest that dietary elements might be one of the key factors beneficially or adversely affecting AD progression (Dohrmann et al, ; Nakagawa et al, ; Perrone & Grant, ).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Quercetin is protective against short‐term dietary advanced glycation end products intake induced cognitive dysfunction in aged ICR mice

et al. 2020

View full text Add to dashboard Cite

Dietary advanced glycation end products (dAGEs) might be potential toxins involved in the pathogenesis of Alzheimer’s disease (AD). Quercetin is a flavonoid possessing neuroprotective effects. We aimed to explore whether a 21 days of dAGEs intake would result in cognitive dysfunction in aged ICR mice, and the protective effects of quercetin, with potential mechanisms explored. Fourteen‐month old ICR mice were randomly assigned into four groups, that is, Control, AGEs, quercetin, and AGE diet supplemented with quercetin. Key markers involved in Aβ, tau, and neuroinflammation from hippocampus and cortex were measured via western blot. Gut microbiota and short chain fatty acids profiles from intestinal contents were measured via 16S rRNA gene sequencing and gas chromatography (GC), respectively. Quercetin alleviated cognitive impairment induced by dAGEs in aged mice. This might be associated with that quercetin reduced cathepsin B, tau phosphorylation, and neuroinflammation, and elevated α‐diversity index (ACE, Chao1, and Shannon index), and reduced phylum Verrucomicrobia of gut microbiota. Practical applications Alzheimer’s disease (AD) has been regarded as the commonest cause of progressive dementia for the elderly. This study is the very first to demonstrate that even a short‐term dietary advanced glycation end product (dAGEs) intake induced impaired cognitive function in aged ICR mice, and querectin is capable of reversing dAGEs‐induced cognitive dysfunction. Reduced tau phosphorylation, neuroinflammation, and altered gut microbiota profiles may be involved in querectin’s protective effects against dAGEs‐induced cognitive impairment. Our study suggested that quercetin supplementation might be beneficial for improving cognitive function in elderly subjects with high consumption of dAGEs such as grilling, frying, and broiling of food.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Quercetin is protective against short‐term dietary advanced glycation end products intake induced cognitive dysfunction in aged ICR mice

et al. 2020

View full text Add to dashboard Cite

show abstract

“…AGEs are prevalent in the diabetic vasculature and contribute to the development of atherosclerosis. Research over the last 30 years has implicated that AGEs are associated with aging and neurodegenerative diseases, including Alzheimer's disease (AD) (Sasaki et al 1998;Takeuchi et al 2004;Galasko et al 2014;Kuhla et al 2014;Perrone and Grant 2015). It has been found that brains of Alzheimer's patients show a high concentration of AGEs compared to normal brains (Takeuchi and Yamagishi 2008;Krautwald and Munch 2010).…”

Section: Introductionmentioning

confidence: 94%

Role of RAGE in Alzheimer’s Disease

et al. 2015

View full text Add to dashboard Cite

Receptor for advanced glycation end products (RAGE) is a receptor of the immunoglobulin super family that plays various important roles under physiological and pathological conditions. Compelling evidence suggests that RAGE acts as both an inflammatory intermediary and a critical inducer of oxidative stress, underlying RAGE-induced Alzheimer-like pathophysiological changes that drive the process of Alzheimer's disease (AD). A critical role of RAGE in AD includes beta-amyloid (Aβ) production and accumulation, the formation of neurofibrillary tangles, failure of synaptic transmission, and neuronal degeneration. The steady-state level of Aβ depends on the balance between production and clearance. RAGE plays an important role in the Aβ clearance. RAGE acts as an important transporter via regulating influx of circulating Aβ into brain, whereas the efflux of brain-derived Aβ into the circulation via BBB is implemented by LRP1. RAGE could be an important contributor to Aβ generation via enhancing the activity of β- and/or γ-secretases and activating inflammatory response and oxidative stress. However, sRAGE-Aβ interactions could inhibit Aβ neurotoxicity and promote Aβ clearance from brain. Meanwhile, RAGE could be a promoting factor for the synaptic dysfunction and neuronal circuit dysfunction which are both the material structure of cognition, and the physiological and pathological basis of cognition. In addition, RAGE could be a trigger for the pathogenesis of Aβ and tau hyper-phosphorylation which both participate in the process of cognitive impairment. Preclinical and clinical studies have supported that RAGE inhibitors could be useful in the treatment of AD. Thus, an effective measure to inhibit RAGE may be a novel drug target in AD.

show abstract

“…A similar decline was also found in a longer study (up to 84 months) (West et al 2014) suggesting a diet low in AGE may protect against age-related cognitive decline and reduce dementia risk. Looking at AD specifically, Perrone and Grant (2015) assessed the AGE content of diets from cohort studies which correlated diet and AD incidence. The authors concluded that dietary AGE content is a risk factor for AD, and that long-term restriction studies are now needed.…”

Section: Whole Dietmentioning

confidence: 99%