The neuroprotective effects of caffeine

Ritchie, Karen; Carrière, Isabelle; Mendonça, Alexandre de; Portet, Florence; Dartigues, Jean François; Rouaud, Olivier; Barberger‐Gateau, Pascale; Ancelin, Marie-Laure

doi:10.1212/01.wnl.0000266670.35219.0c

Cited by 318 publications

(291 citation statements)

References 24 publications

Supporting

Mentioning

260

Contrasting

Unclassified

Order By: Relevance

“…Fasting blood samples were taken at baseline for lipid and glucose levels and APOE4 genotyping (Ritchie et al, 2007). History of ischemic pathologies (stroke, angina pectoris, myocardial infarction and cardio-vascular surgery) was established according to standardized questions.…”

Section: Socio-demographic and Clinical Variablesmentioning

confidence: 99%

“…Multivariate adjusted logistic regression further included covariates associated with cognitive decline (at p<0.15); depression, diabetes, hypercholesterolemia, caffeine, smoking, APOE4, ischemic pathologies, chronic joint or back pain, bronchitis, asthma and other chronic respiratory disorders. Due to the skewed distribution of cognitive scores, a substantial decline in cognitive function over follow-up was defined as the lowest quintile of the difference between either follow-up visit and baseline score except for response time recorded for the TMT, for which the highest quintile of the difference was considered (Ritchie et al, 2007). We also used random-effect models to analyze the association between CS use and 7-year change on cognitive scores taken as continuous variables.…”

Section: Statistical Analysesmentioning

confidence: 99%

See 1 more Smart Citation

Steroid and nonsteroidal anti-inflammatory drugs, cognitive decline, and dementia

Ancelin

Carrière

Helmer

et al. 2012

Neurobiology of Aging

View full text Add to dashboard Cite

Section: Socio-demographic and Clinical Variablesmentioning

confidence: 99%

Section: Statistical Analysesmentioning

confidence: 99%

Steroid and nonsteroidal anti-inflammatory drugs, cognitive decline, and dementia

Ancelin

Carrière

Helmer

et al. 2012

Neurobiology of Aging

View full text Add to dashboard Cite

“…Eskelinen et al (2009) reported a 65 % risk reduction for late-life dementia and AD among drinkers of three to five cups of coffee per day during their middle life, compared with nondrinkers. The caffeine in coffee has been implicated as the active component associated with risk reduction of cognitive decline and dementia among coffee drinkers (Maia and de Mendonca 2002;van Gelder et al 2007), particularly among women (Ritchie et al 2007;Santos et al 2010). However, coffee also contains a variety of other bioavailable and potentially therapeutic phytochemicals.…”

Section: Introductionmentioning

confidence: 99%

Coffee, but not caffeine, has positive effects on cognition and psychomotor behavior in aging

Shukitt‐Hale

Miller

Chu

et al. 2013

AGE

View full text Add to dashboard Cite

The complex mixture of phytochemicals in fruits and vegetables provides protective health benefits, mainly through additive and/or synergistic effects. The presence of several bioactive compounds, such as polyphenols and caffeine, implicates coffee as a potential nutritional therapeutic in aging. Moderate (three to five cups a day) coffee consumption in humans is associated with a significant decrease in the risk of developing certain chronic diseases. However, the ability of coffee supplementation to improve cognitive function in aged individuals and the effect of the individual components in coffee, such as caffeine, have not been fully evaluated. We fed aged rats (19 months) one of five coffeesupplemented diets (0, 0.165, 0.275, 0.55, and 0.825 % of the diet) for 8 weeks prior to motor and cognitive behavior assessment. Aged rats supplemented with a 0.55 % coffee diet, equivalent to ten cups of coffee, performed better in psychomotor testing (rotarod) and in a working memory task (Morris water maze) compared to aged rats fed a control diet. A diet with 0.55 % coffee appeared to be optimal. The 0.165 % coffeesupplemented group (three cups) showed some improvement in reference memory performance in the Morris water maze. In a subsequent study, the effects of caffeine alone did not account for the performance improvements, showing that the neuroprotective benefits of coffee are not due to caffeine alone, but rather to other bioactive compounds in coffee. Therefore, coffee, in achievable amounts, may reduce both motor and cognitive deficits in aging.

show abstract

“…Human epidemiological and animal experimentation studies as well as studies conducted in cultured cell models have shown that caffeine protects against the onset and severity of AD [19][20][21][22][23][24][25][26][27][28]. Additionally, it has been shown that it can reverse behavioral and pathological features of AD [19,21,22,24,25,[29][30][31][32][33].…”

Section: Introductionmentioning

confidence: 99%

“…Additionally, it has been shown that it can reverse behavioral and pathological features of AD [19,21,22,24,25,[29][30][31][32][33]. Importantly, these protective effects of caffeine are observed using pharmacologically relevant doses [28,34].…”

Section: Introductionmentioning

confidence: 99%

Caffeine blocks cholesterol-enriched diet induced AD-like pathology in rabbits

Chen¹,

Tian²,

Ghribi³

et al. 2016

J Integr Syst Neurosci

View full text Add to dashboard Cite

The pathogenesis of sporadic AD is believed to result from complex interactions between nutritional, environmental, epigenetic and genetic factors. Among those factors, elevated plasma cholesterol, independent of APOE genotypes, is strongly linked to the pathogenesis of sporadic AD, whereas chronic ingestion of caffeine is protective against sporadic AD. Others and we have shown that rabbits-fed cholesterol-enriched diet exhibit early AD-like pathological features including bloodbrain barrier (BBB) leakage and endolysosome dysfunction, as well as, AD-like pathological hallmarks including synaptic disruption, increased intraneuronal and brain deposition of amyloid beta (Aβ), and tau pathology. Further, we found that caffeine protects against the cholesterol-induced increases in BBB permeability. Here, we determined the extent to which caffeine affects cholesterol-enriched diet-induced increases in other pathological features of AD. We demonstrated that caffeine administration at low and moderate doses did not affect plasma levels of cholesterol, but did block significantly cholesterol-enriched diet-induced increases in brain levels of apoB and accumulation of apoB in neuronal endolysosomes. Furthermore, we demonstrated that caffeine administration at the two doses blocked cholesterol-enriched diet-induced abnormal accumulation of synaptophysin, Aβ, and phosphorylated tau in endolysosomes. Our findings suggest that caffeine exerts its protective effects against the development of sporadic AD-like pathological features, in part, by preventing the entrance of LDL cholesterol into brain parenchyma, the accumulation of LDL-cholesterol in neuronal endolysosomes, and structural and functional changes to endolysosomes.

show abstract

The neuroprotective effects of caffeine

Cited by 318 publications

References 24 publications

Steroid and nonsteroidal anti-inflammatory drugs, cognitive decline, and dementia

Steroid and nonsteroidal anti-inflammatory drugs, cognitive decline, and dementia

Coffee, but not caffeine, has positive effects on cognition and psychomotor behavior in aging

Caffeine blocks cholesterol-enriched diet induced AD-like pathology in rabbits

Contact Info

Product

Resources

About