Corrigendum to “Central insulin dysregulation and energy dyshomeostasis in two mouse models of Alzheimer’s disease” [Neurobiol. Aging 58 (2017) 1–13]

Velázquez, Ramón; Tran, An; Ishimwe, Egide; Denner, Larry; Dave, Nikhil; Oddo, Salvatore; Dineley, Kelly T.

doi:10.1016/j.neurobiolaging.2017.08.011

Cited by 1 publication

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“…Besides, accumulating evidences showed that impaired insulin signaling pathway was also associated with cognitive dysfunction. [57] Mi et al illustrated epigallocatechin-3-gallate alleviated cognitive deficit by regulating the IRS/AKT and MAPK/CREB/BDNF. [14] AKT and MAPK, as downstream proteins in insulin signaling, were correlated with neuron growth and memory.…”

Section: Discussionmentioning

confidence: 99%

Quercetin‐3‐O‐Glucuronide Alleviates Cognitive Deficit and Toxicity in Aβ_1‐42‐Induced AD‐Like Mice and SH‐SY5Y Cells

Mei-ling

Huang

et al. 2021

Molecular Nutrition Food Res

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Scope Alzheimer's disease (AD) is characterized by amyloid‐β (Aβ) related imbalance, Tau‐hyperphosphorylation, and neuroinflammation, in which Aβ and neuroinflammation can induce brain insulin resistance (IR). Gut microbiome disorder is correlated with inflammation in AD. As of yet, there are no effective treatments clinically. Thus, it is focused on the potential benefit of quercetin‐3‐O‐glucuronide (Q3G), a pharmacologically active flavonol glucuronide, on AD treatment by regulating brain IR and the gut microbiome. Methods and results AD mice model built through intracerebroventricular injection of Aβ1‐42 and AD cell model developed through the SH‐SY5Y cell line and Aβ1‐42 are used to explore the protective effects of Q3G on AD. Neurobehavioral test, brain insulin signaling pathway, and high‐throughput pyrosequencing of 16S rRNA are assessed. Data show that Q3G attenuates neuroinflammation and brain IR in Aβ1‐42‐injected mice and relieves apoptosis in Aβ1‐42‐treated SH‐SY5Y cells by interrupting the downstream insulin signaling. Q3G ameliorates Aβ accumulation and Tau phosphorylation, restores CREB and BDNF levels in the hippocampus , and reverses Aβ1‐42‐induced cognitive impairment. Besides, Q3G restores Aβ1‐42‐induced reduction of short‐chain fatty acids (SCFAs) and gut microbiota dysbiosis. Conclusion Q3G can alleviate brain IR through directly acting on the brain or modulating the gut‐brain axis, ultimately to relieve Aβ1‐42‐induced cognitive dysfunction.

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Section: Discussionmentioning

confidence: 99%

Quercetin‐3‐O‐Glucuronide Alleviates Cognitive Deficit and Toxicity in Aβ_1‐42‐Induced AD‐Like Mice and SH‐SY5Y Cells

Mei-ling

Huang

et al. 2021

Molecular Nutrition Food Res

View full text Add to dashboard Cite

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Corrigendum to “Central insulin dysregulation and energy dyshomeostasis in two mouse models of Alzheimer’s disease” [Neurobiol. Aging 58 (2017) 1–13]

Cited by 1 publication

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Quercetin‐3‐O‐Glucuronide Alleviates Cognitive Deficit and Toxicity in Aβ_1‐42‐Induced AD‐Like Mice and SH‐SY5Y Cells

Quercetin‐3‐O‐Glucuronide Alleviates Cognitive Deficit and Toxicity in Aβ_1‐42‐Induced AD‐Like Mice and SH‐SY5Y Cells

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Corrigendum to “Central insulin dysregulation and energy dyshomeostasis in two mouse models of Alzheimer’s disease” [Neurobiol. Aging 58 (2017) 1–13]

Cited by 1 publication

References 0 publications

Quercetin‐3‐O‐Glucuronide Alleviates Cognitive Deficit and Toxicity in Aβ1‐42‐Induced AD‐Like Mice and SH‐SY5Y Cells

Quercetin‐3‐O‐Glucuronide Alleviates Cognitive Deficit and Toxicity in Aβ1‐42‐Induced AD‐Like Mice and SH‐SY5Y Cells

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Product

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About

Quercetin‐3‐O‐Glucuronide Alleviates Cognitive Deficit and Toxicity in Aβ_1‐42‐Induced AD‐Like Mice and SH‐SY5Y Cells

Quercetin‐3‐O‐Glucuronide Alleviates Cognitive Deficit and Toxicity in Aβ_1‐42‐Induced AD‐Like Mice and SH‐SY5Y Cells