Roasted Coffee Reduces β‐Amyloid Production by Increasing Proteasomal β‐Secretase Degradation in Human Neuroblastoma SH‐SY5Y Cells

Fukuyama, Kazuya; Kakio, Shota; Nakazawa, Yosuke; Kobata, Kenji; Funakoshi‐Tago, Megumi; Suzuki, Toshiharu; Tamura, Hiroomi

doi:10.1002/mnfr.201800238

Cited by 20 publications

(6 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this context, e.g., a recent study by Fukuyama et al is highly interesting. Fukuyama et al addressed the effect of roasted coffee and its naturally occurring compounds on amyloidogenic β-secretase processing of APP [79]. In line with our findings, they observed by testing roasted coffee (including caffeine, caffeic acid, chlorogenic acid and trigonelline) a reduced BACE1 protein expression accompanied by reduced secreted Aβ level.…”

Section: Discussionsupporting

confidence: 89%

Effect of Caffeine and Other Methylxanthines on Aβ-Homeostasis in SH-SY5Y Cells

et al. 2019

View full text Add to dashboard Cite

Methylxanthines (MTX) are alkaloids derived from the purine-base xanthine. Whereas especially caffeine, the most prominent known MTX, has been formerly assessed to be detrimental, this point of view has changed substantially. MTXs are discussed to have beneficial properties in neurodegenerative diseases, however, the mechanisms of action are not completely understood. Here we investigate the effect of the naturally occurring caffeine, theobromine and theophylline and the synthetic propentofylline and pentoxifylline on processes involved in Alzheimer’s disease (AD). All MTXs decreased amyloid-β (Aβ) level by shifting the amyloid precursor protein (APP) processing from the Aβ-producing amyloidogenic to the non-amyloidogenic pathway. The α-secretase activity was elevated whereas β-secretase activity was decreased. Breaking down the molecular mechanism, caffeine increased protein stability of the major α-secretase ADAM10, downregulated BACE1 expression and directly decreased β-secretase activity. Additionally, APP expression was reduced. In line with literature, MTXs reduced oxidative stress, decreased cholesterol and a decreased in Aβ1-42 aggregation. In conclusion, all MTXs act via the pleiotropic mechanism resulting in decreased Aβ and show beneficial properties with respect to AD in neuroblastoma cells. However, the observed effect strength was moderate, suggesting that MTXs should be integrated in a healthy diet rather than be used exclusively to treat or prevent AD.

show abstract

Section: Discussionsupporting

confidence: 89%

Effect of Caffeine and Other Methylxanthines on Aβ-Homeostasis in SH-SY5Y Cells

et al. 2019

View full text Add to dashboard Cite

show abstract

“…In addition, the beneficial effect of caffeine on Aβ could be associated with antagonism of NMDA receptors or agonism of RyRs [165]. Moreover, brewed coffee reduced Aβ production by a decrease in BACE-1 expression (which was not associated with caffeine activity) in human neuroblastoma SH-SY5Y cells [184]. Brewed coffee increased expression of vascular endothelial growth factor (VEGF)in SH-SY5Y cells, indicating possible neuroprotective effect [185].…”

Section: Discussionmentioning

confidence: 99%

Potential of Caffeine in Alzheimer’s Disease—A Review of Experimental Studies

et al. 2021

View full text Add to dashboard Cite

Alzheimer’s disease (AD) is the most common type of dementia leading to progressive memory loss and cognitive impairment. Considering that pharmacological treatment options for AD are few and not satisfactory, increasing attention is being paid to dietary components that may affect the development of the disease. Such a dietary component may be caffeine contained in coffee, tea or energy drinks. Although epidemiological data suggest that caffeine intake may counteract the development of cognitive impairment, results of those studies are not conclusive. The aim of the present study is to review the existing experimental studies on the efficacy of caffeine against AD and AD-related cognitive impairment, focusing on the proposed protective mechanisms of action. In conclusion, the reports of studies on experimental AD models generally supported the notion that caffeine may exert some beneficial effects in AD. However, further studies are necessary to elucidate the role of caffeine in the effects of its sources on cognition and possibly AD risk.

show abstract

“…Although caffeine is among hundreds of bioactive compounds in coffee 46 , it is the most widely studied ingredient against Aβ pathology 16–18 . Other bioactive compounds include chlorogenic acid, polyphenols, small amount of minerals, and vitamin B 3 , which have also been investigated 47–49 . However, it remains controversial whether a single ingredient in coffee is effective against Aβ pathology or whether a combination of ingredients is effective.…”

Section: Discussionmentioning

confidence: 99%

Coffee intake and decreased amyloid pathology in human brain

Kim

Byun

et al. 2019

Transl Psychiatry

View full text Add to dashboard Cite

Several epidemiological and preclinical studies supported the protective effect of coffee on Alzheimer’s disease (AD). However, it is still unknown whether coffee is specifically related with reduced brain AD pathologies in human. Hence, this study aims to investigate relationships between coffee intake and in vivo AD pathologies, including cerebral beta-amyloid (Aβ) deposition, the neurodegeneration of AD-signature regions, and cerebral white matter hyperintensities (WMH). A total of 411 non-demented older adults were included. Participants underwent comprehensive clinical assessment and multimodal neuroimaging including [11C] Pittsburgh compound B-positron emission tomography (PET), [18F] fluorodeoxyglucose PET, and magnetic resonance imaging scans. Lifetime and current coffee intake were categorized as follows: no coffee or <2 cups/day (reference category) and ≥2 cups/day (higher coffee intake). Lifetime coffee intake of ≥2 cups/day was significantly associated with a lower Aβ positivity compared to coffee intake of <2 cups/day, even after controlling for potential confounders. In contrast, neither lifetime nor current coffee intake was not related to hypometabolism, atrophy of AD-signature region, and WMH volume. The findings suggest that higher lifetime coffee intake may contribute to lowering the risk of AD or related cognitive decline by reducing pathological cerebral amyloid deposition.

show abstract

Roasted Coffee Reduces β‐Amyloid Production by Increasing Proteasomal β‐Secretase Degradation in Human Neuroblastoma SH‐SY5Y Cells

Abstract: The data suggest that the roasting process may be crucial for the protective effects of coffee consumption in AD.

Cited by 20 publications

References 26 publications

Effect of Caffeine and Other Methylxanthines on Aβ-Homeostasis in SH-SY5Y Cells

Effect of Caffeine and Other Methylxanthines on Aβ-Homeostasis in SH-SY5Y Cells

Potential of Caffeine in Alzheimer’s Disease—A Review of Experimental Studies

Coffee intake and decreased amyloid pathology in human brain

Contact Info

Product

Resources

About