Effects of (âˆ’)Epicatechin on the Pathology of APP/PS1 Transgenic Mice

Yue-Qin, Zeng; Wang, Yan‐Jiang; Zhou, Xin‐Fu

doi:10.3389/fneur.2014.00069

Cited by 33 publications

(20 citation statements)

References 45 publications

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“…In a previous study, Zeng and colleagues (2014) [101] demonstrated the grape seed extract (GSE) could reduce brain amyloid-β burden and microglia activation, but which polyphenol plays a major role in these events is not known. They tested pharmacological effects of (−) epicatechin, one principle polyphenol compound in GSE, on transgenic AD mice.…”

Section: Research On Curcumin In Mouse Models Of Alzheimer’s Diseasementioning

confidence: 99%

“…The (−) epicatechin diet did not alter learning and memory behaviors in AD mice. This study has provided evidence on the beneficial role of (−) epicatechin in ameliorating amyloid-induced AD-like pathology in AD mice, but the impact of (−) epicatechin on tau pathology is not clear, also the mechanism needs further research [101]. …”

Section: Research On Curcumin In Mouse Models Of Alzheimer’s Diseasementioning

confidence: 99%

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Protective Effects of Indian Spice Curcumin Against Amyloid-β in Alzheimer’s Disease

Reddy

Mańczak

Yin

et al. 2018

JAD

274

138

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The purpose of our article is to assess the current understanding of Indian spice ‘Curcumin’ against amyloid-β (Aβ)-induced toxicity in Alzheimer’s disease (AD) pathogenesis. Natural products, such as ginger, curcumin and gingko biloba have been used as diets and dietary supplements to treat human diseases, including cancer, cardiovascular, respiratory, infectious, diabetes, obesity, metabolic syndromes and neurological disorders. Products derived from plants are known to have protective effects, including anti-inflammatory, anti-oxidant, anti-arthritis, pro-healing and boosting memory cognitive functions. In the last decade, several groups have designed and synthesized curcumin and its derivatives and extensively tested using cell and mouse models of AD. Recent research on amyloid-β and curcumin has revealed that curcumin prevents amyloid-β aggregation and crosses the blood brain barrier (BBB), reach brain cells and protect neurons from various toxic insults of aging and amyloid-β in humans. Recent research has also reported that curcumin ameliorates cognitive decline and improves synaptic functions in mouse models of AD. Further, recent groups have initiated studies on elderly individuals and patients with AD and the outcome of these studies is currently being assessed. This article highlights the beneficial effects of curcumin on AD. This article also critically assesses the current limitations of curcumin’s bioavailability and urgent need for new formulation to increase its brain levels to treat patients with AD.

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Section: Research On Curcumin In Mouse Models Of Alzheimer’s Diseasementioning

confidence: 99%

Section: Research On Curcumin In Mouse Models Of Alzheimer’s Diseasementioning

confidence: 99%

Protective Effects of Indian Spice Curcumin Against Amyloid-β in Alzheimer’s Disease

Reddy

Mańczak

Yin

et al. 2018

JAD

274

138

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“…[ 9 ] In the amyloid precursor protein/presenilin 1 (APP/PS1) mice model, epicatechin significantly inhibited the deposits of amyloid in the brain and reduced the levels of Aβ in the blood, with no adverse event. [ 11 ] Moreover, epicatechin appears to be well tolerated in relation to viability and systemic toxicity by APP/PS1 mice. Although these studies suggest a promising future for epicatechin application, there have been inconsistencies[ 12 ] in findings and lack of a systematic approach to discover the underlying mechanism.…”

Section: Introductionmentioning

confidence: 99%

Epicatechin plus treadmill exercise are neuroprotective against moderate-stage amyloid precursor protein/presenilin 1 mice

Zhang¹,

Wu²,

Huang³

2016

Phcog Mag

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Background:Epidemiological evidence suggests that exercise and dietary polyphenols are beneficial in reducing Alzheimer's disease (AD) risk.Materials and Methods:In the present study, 8 months old amyloid precursor protein/presenilin 1 (APP/PS1) mice (a moderate pathology phase) were given the green tea catechin (-)-epicatechin delivered orally in the drinking water (50 mg/kg daily), along with treadmill exercise for 4 months, in order to investigate whether the combination can ameliorate the cognitive loss and delay the progression of AD in APP/PS1 transgenic (Tg) mice.Results:At termination, untreated-Tg mice showed elevated soluble amyloid-β (Aβ1–40) and Aβ1–42 levels and deficits in spatial learning and memory, compared with their wild-type littermates. The combined intervention protected against cognitive deficits in the Morris water maze, lowered soluble Aβ1–40 and Aβ1–42 levels in the hippocampus as well as reducing brain oxidative stress. In addition, brain-derived neurotrophic factor proteins wee elevated and Akt/GSK-3/cAMP response element-binding protein signaling was activated in the combination group.Conclusions:Dietary polyphenol plus exercise may exert beneficial effects on brain health and slow the progression of moderate- or mid-stages of AD.SUMMARY Amyloid precursor protein/presenilin 1 transgenic mice showed elevated soluble amyloid-β (Aβ1–40) and Aβ1–42 levels and deficits in spatial learning and memory, compared with their wild-type littermatesOral administration of epicatechin, combined with treadmill exercise for 4 months, could protect against cognitive deficits, and lowered soluble Aβ1–40 and Aβ1–42 levels as well as reducing brain oxidative stressBrain-derived neurotrophic factor proteins were elevated, and Akt/GSK-3/cAMP response element binding protein signaling was activated in the combination groupDietary polyphenol plus exercise might exert beneficial effects on brain health and slow the progression of moderate- or mid-stages of Alzheimer's disease. Abbreviations used: AD: Alzheimer's disease, Tg: APP/PS1 transgenic, BDNF: Brain-derived neurotrophic factor, Aβ: Amyloid-β, APP: Amyloid precursor protein, PS1: Presenilin 1, nTg: Wild-type littermates, IACUC: Institutional Animal Care and Use Committee, GSSG: Glutathione oxidized form, GSH: Glutathione reductase, SOD: Superoxide dismutase, CAT: Catalase, LPO: Lipoperoxidation, CREB: cAMP response element binding protein.

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“… 9 , 10 The active ingredient that confers these benefits often remains unclear, as most investigations examine whole foods or multiple flavanols 11 , 12 , 13 , 14 in animal models of aging, 15 , 16 cerebrovascular stress 17 or Alzheimer's disease. 18 , 19 , 20 , 21 , 22 As such, a pure flavanol of particular interest is (−)epicatechin (EC), which traverses the blood–brain barrier and may directly affect brain function. 22 , 23 , 24 EC consumption improves memory in mice 24 and snails.…”

Section: Introductionmentioning

confidence: 99%

Plant-derived flavanol (−)epicatechin mitigates anxiety in association with elevated hippocampal monoamine and BDNF levels, but does not influence pattern separation in mice

et al. 2015

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Flavanols found in natural products such as cocoa and green tea elicit structural and biochemical changes in the hippocampus, a brain area important for mood and cognition. Here, we evaluated the outcome of daily consumption of the flavanol (−)epicatechin (4 mg per day in water) by adult male C57BL/6 mice on measures of anxiety in the elevated plus maze (EPM) and open field (OF). Furthermore, pattern separation, the ability to distinguish between closely spaced identical stimuli, considered to be mediated by the hippocampal dentate gyrus (DG), was tested using the touchscreen. To investigate mechanisms through which (−)epicatechin may exert its effects, mice were injected with bromodeoxyuridine (50 mg kg−1) to evaluate adult hippocampal neurogenesis. In addition, monoaminergic and neurotrophin signaling pathway proteins were measured in tissue derived from subject cortices and hippocampi. Flavanol consumption reduced anxiety in the OF and EPM. Elevated hippocampal and cortical tyrosine hydroxylase, downregulated cortical monoamine oxidase-A levels, as well as increased hippocampal brain-derived neurotrophic factor (BDNF) and pro-BDNF support the flavanol's anxiolytic effects. In addition, elevated pAkt in hippocampus and cortex was observed. (−)Epicatechin ingestion did not facilitate touchscreen performance or DG neurogenesis, suggesting a non-neurogenic mechanism. The concurrent modulation of complementary neurotrophic and monoaminergic signaling pathways may contribute to beneficial mood-modulating effects of this flavanol.

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Effects of (âˆ’)Epicatechin on the Pathology of APP/PS1 Transgenic Mice

Cited by 33 publications

References 45 publications

Protective Effects of Indian Spice Curcumin Against Amyloid-β in Alzheimer’s Disease

Protective Effects of Indian Spice Curcumin Against Amyloid-β in Alzheimer’s Disease

Epicatechin plus treadmill exercise are neuroprotective against moderate-stage amyloid precursor protein/presenilin 1 mice

Plant-derived flavanol (−)epicatechin mitigates anxiety in association with elevated hippocampal monoamine and BDNF levels, but does not influence pattern separation in mice

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