Anthocyanin-enriched bilberry and blackcurrant extracts modulate amyloid precursor protein processing and alleviate behavioral abnormalities in the APP/PS1 mouse model of Alzheimer's disease

Vepsäläinen, Saila; Koivisto, Hennariikka; Pekkarinen, E.; Mäkinen, Petra; Dobson, Gary; McDougall, Gordon J.; Stewart, Derek; Haapasalo, Annakaisa; Karjalainen, Reijo; Tanila, Heikki; Hiltunen, Mikko

doi:10.1016/j.jnutbio.2012.07.006

Cited by 128 publications

(81 citation statements)

References 36 publications

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“…In this regard, it was recently demonstrated that anthocyanin-enriched bilberry and black currant extracts have the ability to modulate APP processing and alleviate behavioral abnormalities in the APP/PS1 mouse model of AD. 60 In the transgenic PSAPP mouse model of cerebral amyloidosis, oral administration of tannic acid for 6 months prevented transgene-associated behavioral impairment and defective spatial reference memory. Several other studies further support the efficacy of flavonoids on memory and learning, as for example, nobiletin, a citrus flavonoid, which proved to ameliorate Aβ-induced memory impairment and decrease the Aβ burden and plaques in the hippocampus of a transgenic mouse model of AD.…”

Section: ■ Flavonoidsmentioning

confidence: 99%

Flavonoids as Therapeutic Compounds Targeting Key Proteins Involved in Alzheimer’s Disease

Baptista

Henriques

Silva

et al. 2014

ACS Chem. Neurosci.

162

111

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Alzheimer's disease is characterized by pathological aggregation of protein tau and amyloid-β peptides, both of which are considered to be toxic to neurons. Naturally occurring dietary flavonoids have received considerable attention as alternative candidates for Alzheimer's therapy taking into account their antiamyloidogenic, antioxidative, and anti-inflammatory properties. Experimental evidence supports the hypothesis that certain flavonoids may protect against Alzheimer's disease in part by interfering with the generation and assembly of amyloid-β peptides into neurotoxic oligomeric aggregates and also by reducing tau aggregation. Several mechanisms have been proposed for the ability of flavonoids to prevent the onset or to slow the progression of the disease. Some mechanisms include their interaction with important signaling pathways in the brain like the phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase pathways that regulate prosurvival transcription factors and gene expression. Other processes include the disruption of amyloid-β aggregation and alterations in amyloid precursor protein processing through the inhibition of β-secretase and/or activation of α-secretase, and inhibiting cyclin-dependent kinase-5 and glycogen synthase kinase-3β activation, preventing abnormal tau phosphorylation. The interaction of flavonoids with different signaling pathways put forward their therapeutic potential to prevent the onset and progression of Alzheimer's disease and to promote cognitive performance. Nevertheless, further studies are needed to give additional insight into the specific mechanisms by which flavonoids exert their potential neuroprotective actions in the brain of Alzheimer's disease patients. KEYWORDS: Flavonoids, Alzheimer's disease, amyloid precursor protein, amyloid beta, BACE-1, tau, signaling A lzheimer's disease (AD) is a neurodegenerative disorder and the most common form of dementia worldwide. The major histopathological hallmarks of AD include proteinous aggregates in the form of neurofibrillary tangles (NFTs), consisting of hyperphosphorylated tau 1,2 and extracellular senile plaques, which are deposits of heterogeneously sized small peptides of amyloid-β (Aβ) that are formed via sequential proteolytic cleavages of the amyloid precursor protein (APP) 3 (Figure 1). Dominant mutations in APP, presenilin-1 (PS1) or PS2 are responsible for the early onset or familial form of AD. These mutations have been shown to profoundly alter APP metabolism, favoring the production of aggregation-prone Aβ species, these findings formed the basis for the "amyloid cascade hypothesis" of AD pathogenesis. This broadly accepted hypothesis states that the generation of neurotoxic Aβ peptides by β-secretase and γ-secretase are at the basis of AD pathophysiology. Other hallmarks of this disease, like neurotransmitter changes 4,5 and neuronal and synapse loss in the neocortex and the hippocampus 6,7 develop as a consequence of this event.■ AMYLOID PRECURSOR PROTEIN APP belongs to a protein f...

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Section: ■ Flavonoidsmentioning

confidence: 99%

Flavonoids as Therapeutic Compounds Targeting Key Proteins Involved in Alzheimer’s Disease

Baptista

Henriques

Silva

et al. 2014

ACS Chem. Neurosci.

162

111

View full text Add to dashboard Cite

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“…Of these, anthocyanins are known to undergo gut microbial conversion into corresponding aglycones or anthocyanidins [7] [8]. Anthocyanin-rich bilberry and blackcurrant diets alleviate behavioral abnormalities in a mouse model of Alzheimer's disease [9]. Further, blackcurrant anthocyanins provide a number of health benefits, including improved blood flow and decreased inflammatory marker levels [10].…”

Section: Introductionmentioning

confidence: 99%

Single Oral Administration of Anthocyanin Rescues Smoking-Induced Endothelial Dysfunction in Young Smokers but Facilitates Oxidative Stress in Non-Smokers

Akane¹,

Tomisawa²,

Osanai³

et al. 2018

FNS

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Objectives: Smoking causes endothelial dysfunction, but it still remains unclear whether oral administration of anthocyanin brings benefits to endothelial function and redox states in young healthy smokers. We tested the hypothesis that supplement anthocyanin may rescue endothelial dysfunction and redox states in young healthy smokers. Methods: Young healthy male non-smoker (n = 8) and smokers (n = 14) were enrolled to measure the derivatives of reactive oxygen metabolites (d-ROMs) and biological antioxidant potential (BAP) levels and brachial artery flow-mediated dilation (FMD) before and 2 hours after one cigarette smoking or resting under administration of blackcurrant supplements (anthocyanins 210 mg) or not. Results: FMD, d-ROMs, and BAP at baseline were similar between non-smokers and smokers. One cigarette smoking induced a decrease in FMD at 2 hours (9.0% ± 2.6% vs 7.5% ± 2.3%, p < 0.05) without affecting plasma levels of d-ROMs and BAP in young healthy smokers. Single oral administration of anthocyanin at 210 mg abolished smoking-induced decrease in FMD (8.3% ± 3.4% vs 9.5% ± 3.6%, p = ns) without changes in plasma levels of d-ROMs and BAP in young smokers. In non-smokers, however, administration of anthocyanin at 210 mg slightly but significantly elevated plasma level of d-ROMs at 2 hours (249.6 ± 30.3 vs How to cite this paper: Yoshizaki, A., Tomisawa, T., Osanai, T., Nanashima, N., Kitajima, M., Mikami, K., Fujita, T., Maeda, H. and Kato, Y. (2018)

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“…Quercetin (a flavonol), followed by myricetin (a flavonol) and kaempferol (a flavonol), and then apigenin (flavone), baicalein (flavone), catechin (flavan-3-ols), and EGCG (flavan-3-ols) are the most studied phenolic compounds. In particular, quercetin has shown several neuroprotective effects, being its ability to reduce and/or to prevent reactive oxygen species (ROS) overproduction amongst to the most prominent; its active concentrations varied significantly according to the model used, but interestingly, as described by Vepsäläinen et al (2013), at 0.5, 2.5, and 10 µM a, pronounced reduction in ROS overproduction was observed in human SH-SY5Y neuroblastoma cells (with menadione as oxidative stress inducer).…”

Section: Plant-food-based Formulations: An Integrative Approachmentioning

confidence: 99%

Neurocognitive Improvement Through Plant Food Bioactives: A Particular Approach to Alzheimer’s Disease

Martins

Ferreira

2017

Food Bioactives

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Anthocyanin-enriched bilberry and blackcurrant extracts modulate amyloid precursor protein processing and alleviate behavioral abnormalities in the APP/PS1 mouse model of Alzheimer's disease

Cited by 128 publications

References 36 publications

Flavonoids as Therapeutic Compounds Targeting Key Proteins Involved in Alzheimer’s Disease

Flavonoids as Therapeutic Compounds Targeting Key Proteins Involved in Alzheimer’s Disease

Single Oral Administration of Anthocyanin Rescues Smoking-Induced Endothelial Dysfunction in Young Smokers but Facilitates Oxidative Stress in Non-Smokers

Neurocognitive Improvement Through Plant Food Bioactives: A Particular Approach to Alzheimer’s Disease

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