Beneficial Role of Coffee and Caffeine in Neurodegenerative Diseases: A Minireview.
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ABSTRACT:
SUBMITTER: Sc Y
PROVIDER: S-EPMC5690364 | biostudies-other | 2016
REPOSITORIES: biostudies-other
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Project description:Background: The literature concerning the effect of coffee and caffeine on Multiple Sclerosis (MS) with focus on fatigue is investigated in this review. Potentially clinically relevant effects were also assessed in studies concerning comparable neurodegenerative diseases, such as Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS). Since the existing studies obtained very inconclusive results, we systematically reviewed these studies to summarize the evidence on the possible effects of coffee and caffeine on those disease entities. Previous studies suggested that coffee and caffeine intake is associated with a reduced risk of developing MS and other neurological diseases. Methods: The PubMed database was searched using the keywords "coffee" OR "caffeine" in combination with keywords for each of the different diseases. Besides the keyword search, we included studies by reference list search. Studies on the effects of coffee and caffeine on the single neurological diseases were included for this review. A total of 51 articles met our inclusion criteria. The reviewed articles assessed the impact of coffee and caffeine on the susceptibility for neurological diseases, as well as the effect of coffee and caffeine on disease progression and possible symptomatic effects like on performance enhancement. Results: Higher intake of coffee and caffeine was associated with a lower risk of developing PD. In some of the MS studies there, is evidence for a similar effect and experimental studies confirmed the positive impact. Interestingly in MS coffee and caffeine may have a stronger impact on disease course compared to effects on disease susceptibility. In ALS no such beneficial effect could be observed in the clinical and experimental studies. Conclusion: This literature assessment revealed that coffee and especially caffeine could have a preventative role in the development of several neurodegenerative diseases if provided in comparatively high doses. The systematic assessment indicates that coffee and caffeine intake must not be considered as a health risk. Additional clinical studies are needed to fully understand how far coffee and caffeine intake should be considered as a potential therapeutic approach for certain disease entities and conditions.
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Project description:Apolipoprotein E (APOE) is a lipid-transport protein abundantly expressed in most neurons in the central nervous system. APOE-dependent alterations of the endocytic pathway can affect different functions. APOE binds to cell-surface receptors to deliver lipids and to the hydrophobic amyloid-? peptide, regulating amyloid-? aggregations and clearances in the brain. Several APOE isoforms with major structural differences were discovered and shown to influence the brain lipid transport, glucose metabolism, neuronal signaling, neuroinflammation, and mitochondrial function. This review will summarize the updated research progress on APOE functions and its role in Alzheimer's disease, Parkinson's disease, cardiovascular diseases, multiple sclerosis, type 2 diabetes mellitus, Type III hyperlipoproteinemia, vascular dementia, and ischemic stroke. Understanding the mutations in APOE, their structural properties, and their isoforms is important to determine its role in various diseases and to advance the development of therapeutic strategies. Targeting APOE may be a potential approach for diagnosis, risk assessment, prevention, and treatment of various neurodegenerative and cardiovascular diseases in humans.
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Project description:Caffeine is the world's most widely used central nervous system stimulant, with approximately 80% consumed in the form of coffee. However, studies that analyze prospectively the relationship between coffee or caffeine consumption and depression risk are scarce.A total of 50,739 US women (mean age, 63 years) free of depressive symptoms at baseline (in 1996) were prospectively followed up through June 1, 2006. Consumption of caffeine was measured from validated questionnaires completed from May 1, 1980, through April 1, 2004, and computed as cumulative mean consumption with a 2-year latency period applied. Clinical depression was defined as self-reported physician-diagnosed depression and antidepressant use. Relative risks of clinical depression were estimated using Cox proportional hazards regression models.During 10 years of follow-up (1996-2006), 2607 incident cases of depression were identified. Compared with women consuming 1 or less cup of caffeinated coffee per week, the multivariate relative risk of depression was 0.85 (95% confidence interval, 0.75-0.95) for those consuming 2 to 3 cups per day and 0.80 (0.64-0.99; P for trend<.001) for those consuming 4 cups per day or more. Multivariate relative risk of depression was 0.80 (95% confidence interval, 0.68-0.95; P for trend=.02) for women in the highest (?550 mg/d) vs lowest (<100 mg/d) of the 5 caffeine consumption categories. Decaffeinated coffee was not associated with depression risk.In this large longitudinal study, we found that depression risk decreases with increasing caffeinated coffee consumption. Further investigations are needed to confirm this finding and to determine whether usual caffeinated coffee consumption can contribute to depression prevention.
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Project description:Habitual coffee and caffeine consumption has been reported to be associated with numerous health outcomes. This perspective focuses on Mendelian Randomization (MR) approaches for determining whether such associations are causal. Genetic instruments for coffee and caffeine consumption are described, along with key concepts of MR and particular challenges when applying this approach to studies of coffee and caffeine. To date, at least fifteen MR studies have investigated the causal role of coffee or caffeine use on risk of type 2 diabetes, cardiovascular disease, Alzheimer's disease, Parkinson's disease, gout, osteoarthritis, cancers, sleep disturbances and other substance use. Most studies provide no consistent support for a causal role of coffee or caffeine on these health outcomes. Common study limitations include low statistical power, potential pleiotropy, and risk of collider bias. As a result, in many cases a causal role cannot confidently be ruled out. Conceptual challenges also arise from the different aspects of coffee and caffeine use captured by current genetic instruments. Nevertheless, with continued genome-wide searches for coffee and caffeine related loci along with advanced statistical methods and MR designs, MR promises to be a valuable approach to understanding the causal impact that coffee and caffeine have in human health.
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