Coffee polyphenols prevent cognitive dysfunction and suppress amyloid β plaques in APP/PS2 transgenic mouse

Ishida, Keiko; Yamamoto, Masaki; Misawa, Kensuke; Nishimura, Hitomi; Misawa, Koichi; Ota, Noriyasu; Shimotoyodome, Akira

doi:10.1016/j.neures.2019.05.001

Cited by 57 publications

(48 citation statements)

References 43 publications

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“…A recent work investigated whether treatment with coffee polyphenols (CPPs) was able to prevent or reduce progressive impairments in memory and cognitive function in APP/PS2 mice, a model of AD. The results showed that CPP treatment prevented cognitive dysfunction by reducing amyloid Aβ plaques in the hippocampus due to the disaggregation of the fibrillar Aβ species into Aβ peptides [116].…”

Section: Rats Caffeic Acidmentioning

confidence: 97%

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Natural Compounds as Beneficial Antioxidant Agents in Neurodegenerative Disorders: A Focus on Alzheimer’s Disease

2019

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The positive role of nutrition in chronic neurodegenerative diseases (NDs) suggests that dietary interventions represent helpful tools for preventing NDs. In particular, diets enriched with natural compounds have become an increasingly attractive, non-invasive, and inexpensive option to support a healthy brain and to potentially treat NDs. Bioactive compounds found in vegetables or microalgae possess special properties able to counteract oxidative stress, which is involved as a triggering factor in neurodegeneration. Here, we briefly review the relevant experimental data on curcuminoids, silymarin, chlorogenic acid, and compounds derived from the microalga Aphanizomenon flos aquae (AFA) which have been demonstrated to possess encouraging beneficial effects on neurodegeneration, in particular on Alzheimer's disease models. and intracellular neurofibrillary tangles (NFTs) [4,5]. Intracellular neurofibrillary tangles are composed of hyperphosphorylated Tau proteins in neurons located particularly in the hippocampus and cerebral cortex regions of the brain. The reduced expression of the brain-derived neurotrophic factor (BDNF), important for neuronal growth and memory functions, also plays a crucial role in AD pathogenesis via formation of senile plaque of Aβ and NFTs. At the molecular level, Aβ induces oxidative stress, inflammation, and mitochondrial dysfunction associated with apoptosis [6,7].Parkinson's disease is characterized by the progressive loss of dopaminergic neurons in the substantia nigra (SN) and formation of Lewy bodies, abnormal intraneuronal aggregates of proteins that include α-synuclein, ubiquitin, and neurofilaments [8]. The pathogenic mechanisms of PD include oxidative stress, mitochondrial and protein dysfunction, inflammation, and apoptosis [9]. In particular, oxidative stress generates ROS which activates glial cells, and activated glial cells generate inflammation that results in mitochondrial dysfunction, and, consequently, dysfunctional mitochondria activate cell death machinery [10].Hence, oxidative stress and mitochondrial damage are common factors involved in the etiopathology of these neurodegenerative diseases [11-13]. Oxidative Stress and NeurodegenerationOxidative stress is characterized by an overproduction of ROS-oxygen-containing molecules known to be highly reactive.Reactive oxygen species are formed in mitochondria during oxidative phosphorylation as a byproduct of normal metabolism. Therefore, modest levels of ROS are normally expected and are considered essential for the regulation of normal cell functions, while excessive ROS production can damage various biological targets, such as DNA, lipids, and proteins, causing serious neurological injury. Because the brain consumes a large amount of molecular oxygen to function properly, the accumulation of damaged biomolecules caused by ROS is high, especially with aging [14]. To limit these cellular damages, brain neurons produce antioxidant defense enzymes, such as superoxide dismutase (SOD), glutathione peroxidase (GPX) and catala...

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Section: Rats Caffeic Acidmentioning

confidence: 97%

“…Prevention of cognitive dysfunction and suppression of amyloid β plaques [116]. Mice Chlorogenic Acid Reduction of mild cognitive impairment and AD risk [117,118].…”

Section: Rats Caffeic Acidmentioning

confidence: 99%

Natural Compounds as Beneficial Antioxidant Agents in Neurodegenerative Disorders: A Focus on Alzheimer’s Disease

2019

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“…Caffeoylquinic acids including chlorogenic acid -Suppress Aβ plaque deposition and prevent associated cognitive dysfunction in an AD model (Ishida et al, 2019) Caffeoyl-,dicaffeoyl-,and feruloyl-quinic acids -Improved some cognitive functions in healthy participants (n = 38; 16 weeks) in an RCT (Saitou et al, 2018) -Improved memory functions in elderly with cognitive decline (n = 6; 6 months; Kato et al, 2018) Coffee (see above)…”

Section: Coffeementioning

confidence: 99%

Role of phytochemicals as nutraceuticals for cognitive functions affected in ageing

Howes

Perry²,

Vásquez-Londoño

et al. 2020

British J Pharmacology

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Cognitive decline can occur with normal ageing and in age‐related brain disorders, such as mild cognitive impairment and dementia, including Alzheimer's disease, with limited pharmacological therapies available. Other approaches to reduce cognitive decline are urgently needed, and so, the role of dietary interventions or nutraceuticals has received much attention in this respect. In this review, we examine the evidence for dietary plants and their chemical constituents as nutraceuticals, relevant to both cognitive decline in normal ageing and in dementia. Pharmacological (in vitro and in vivo), clinical and epidemiological evidence is assessed for both frequently consumed plants and their dietary forms, including tea, coffee, cocoa (chocolate), red wine, grapes, citrus and other fruits; in addition to plants used less frequently in certain diets and those that cross the blurred boundaries between foods, nutraceuticals and medicinal plants. For the latter, turmeric, saffron, sage, rosemary and lemon balm are examples of those discussed. Linked Articles This article is part of a themed section on The Pharmacology of Nutraceuticals. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v177.6/issuetoc

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“…The energy content of the control diet was 4.16 kcal g −1 . The 5-CQA diet comprised the control diet plus 0.8% (w/w) 5-CQA which included the same polyphenolic quantities of caffeoylquinic acids and di-CQAs as those in the 1% CPP diet used in our prior study [30]. The potato starch content was reduced to 60.7% (w/w) to compensate for the addition of 5-CQA.…”

Section: Animals and Dietsmentioning

confidence: 99%

“…In our previous study, we demonstrated that CPP comprising caffeoylquinic acids, feruloylquinic acids, and diCQAs prevented cognitive dysfunction and Aβ deposition in the hippocampi of APP/PS2 mice [30]. APP/PS2 double-transgenic mice are AD models that highly express mutant forms of human Aβ precursor protein (APP) and human presenilin-2 (PS2) [31,32].…”

Section: Introductionmentioning

confidence: 99%

5-Caffeoylquinic Acid Ameliorates Cognitive Decline and Reduces Aβ Deposition by Modulating Aβ Clearance Pathways in APP/PS2 Transgenic Mice

et al. 2020

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The accumulation of amyloid β (Aβ) in the brain is a major pathological feature of Alzheimer’s disease (AD). In our previous study, we demonstrated that coffee polyphenols (CPP) prevent cognitive dysfunction and Aβ deposition in the brain of an APP/PS2 transgenic mouse AD model. The underlying mechanisms, however, remain to be elucidated. Here, we investigated the effects of the chronic administration of 5-caffeoylquinic acid (5-CQA), the most abundant component of CPP, on cognitive dysfunction in APP/PS2 mice to identify the role of CPP in Aβ elimination. Relative to the untreated controls, the mice fed a 5-CQA-supplemented diet showed significant improvements in their cognitive function assessed by Y-maze and novel object recognition tests. Histochemical analysis revealed that 5-CQA substantially reduced Aβ plaque formation and neuronal loss in the hippocampi. Moreover, 5-CQA upregulated the gene encoding low-density lipoprotein receptor-related protein 1, an Aβ efflux receptor, and normalized the perivascular localization of aquaporin 4, which facilitates Aβ clearance along the paravascular pathway. These results suggest that 5-CQA reduces Aβ deposition in the brain by modulating the Aβ clearance pathways and ameliorating cognitive decline and neuronal loss in APP/PS2 mice. Thus, 5-CQA may be effective in preventing cognitive dysfunction in AD.

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Coffee polyphenols prevent cognitive dysfunction and suppress amyloid β plaques in APP/PS2 transgenic mouse

Cited by 57 publications

References 43 publications

Natural Compounds as Beneficial Antioxidant Agents in Neurodegenerative Disorders: A Focus on Alzheimer’s Disease

Natural Compounds as Beneficial Antioxidant Agents in Neurodegenerative Disorders: A Focus on Alzheimer’s Disease

Role of phytochemicals as nutraceuticals for cognitive functions affected in ageing

5-Caffeoylquinic Acid Ameliorates Cognitive Decline and Reduces Aβ Deposition by Modulating Aβ Clearance Pathways in APP/PS2 Transgenic Mice

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