Zie ook artikelen op onze website met de ziekte vsn Alzheimer in de titel.

23 septemberr 2925: Bron:  2021 Nov 19;13:744872

Uit een Australische studie naar ontstaan en verloop van de ziekte van Alzheimer blijkt bij 227 volwassen ouderen (60-plus) dat koffieconsumptie een beschermende factor kan zijn tegen de ziekte van Alzheimer. Zoals de auteurs schrijven in het studierapport kan een verhoogde koffieconsumptie de cognitieve achteruitgang mogelijk verminderen door de cerebrale Aβ-amyloïde opbouw te vertragen en zo de bijbehorende neurotoxiciteit van Aβ-amyloïde-gemedieerde oxidatieve stress en ontstekingsprocessen te verminderen. In eenvoudiger woorden de koffie zou de opbouw van de zogeheten seniele plaques die de belangrijkste factor is van de ziekte van Alzheimer vertragen.

Nu is natuurlijk een studie bij 227 mensen niet heel erg groot maar de auteurs vonden hun bevindingen opgemaakt na 126 maanden toch opmerkelijk om deze te publiceren. Deze studie is onderdeel van de veel grotere langjarige Australian Imaging, Biomarkers, and Lifestyle (AIBL) study naar de ziekte van Alzheimer.

Het volledige studierapport is gratis in te zien of te downloaden. Klik daarvoor op de titel van het abstract:

Abstract

Background: Worldwide, coffee is one of the most popular beverages consumed. Several studies have suggested a protective role of coffee, including reduced risk of Alzheimer’s disease (AD). However, there is limited longitudinal data from cohorts of older adults reporting associations of coffee intake with cognitive decline, in distinct domains, and investigating the neuropathological mechanisms underpinning any such associations.

Methods: The aim of the current study was to investigate the relationship between self-reported habitual coffee intake, and cognitive decline assessed using a comprehensive neuropsychological battery in 227 cognitively normal older adults from the Australian Imaging, Biomarkers, and Lifestyle (AIBL) study, over 126 months. In a subset of individuals, we also investigated the relationship between habitual coffee intake and cerebral Aβ-amyloid accumulation (n = 60) and brain volumes (n = 51) over 126 months.

Results: Higher baseline coffee consumption was associated with slower cognitive decline in executive function, attention, and the AIBL Preclinical AD Cognitive Composite (PACC; shown reliably to measure the first signs of cognitive decline in at-risk cognitively normal populations), and lower likelihood of transitioning to mild cognitive impairment or AD status, over 126 months. Higher baseline coffee consumption was also associated with slower Aβ-amyloid accumulation over 126 months, and lower risk of progressing to “moderate,” “high,” or “very high” Aβ-amyloid burden status over the same time-period. There were no associations between coffee intake and atrophy in total gray matter, white matter, or hippocampal volume.

Discussion: Our results further support the hypothesis that coffee intake may be a protective factor against AD, with increased coffee consumption potentially reducing cognitive decline by slowing cerebral Aβ-amyloid accumulation, and thus attenuating the associated neurotoxicity from Aβ-amyloid-mediated oxidative stress and inflammatory processes. Further investigation is required to evaluate whether coffee intake could be incorporated as a modifiable lifestyle factor aimed at delaying AD onset.

On this page

Data Availability Statement

The datasets presented in this article are not readily available because the AIBL data are available only to authorized users. Requests to access the datasets should be directed to the following online form: https://ida.loni.usc.edu/collaboration/access/appApply.jsp?project=AIBL.

Ethics Statement

The study involving human participants was reviewed and approved by the Ethics Commitees of Hollywood Private Hospital, Edith Cowan University, St Vincent’s Health and Austin Health. The patients/participants provided their written informed consent to participate in this study.

Author Contributions

SG, SR-S, KT, CM, PM, CR, DA, and RM designed research. SG conducted research, primary responsibility for final content, and analysis for the manuscript. VV, JF, VD, and PB oversaw collection of and analyzed imaging data. SG and SR-S wrote the manuscript. VV, JF, VD, PB, KT, CF, CM, PM, CR, DA, and RM edited the final manuscript. All authors have read and approved the final manuscript.

Conflict of Interest

VV has served as a consultant for IXICO. CM is an advisor to Prana Biotechnology Ltd., and a consultant to Eli Lilly. PM is a full-time employee of Cogstate Ltd. CR has served on scientific advisory boards for Bayer Pharma, Elan Corporation, GE Healthcare, and AstraZeneca, has received speaker honoraria from Bayer Pharma and GE Healthcare, and has received research support from Bayer Pharma, GE Healthcare, Piramal Lifesciences and Avid Radiopharmaceuticals. RM is founder of, and owns stock in, Alzhyme, and is a co-founder of the KaRa Institute of Neurological Diseases. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher’s Note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Funding

The AIBL study (www.AIBL.csiro.au) is a consortium between Austin Health, CSIRO, Edith Cowan University, the Florey Institute (The University of Melbourne), and the National Ageing Research Institute. The study has received partial financial support from the Alzheimer’s Association (US), the Alzheimer’s Drug Discovery Foundation, an Anonymous foundation (a philanthropic foundation based in the US; one of the conditions of the funding is maintenance of anonymity), the Science and Industry Endowment Fund, the Dementia Collaborative Research Centres, the Victorian Government’s Operational Infrastructure Support program, the Australian Alzheimer’s Research Foundation, the National Health and Medical Research Council (NHMRC), and The Yulgilbar Foundation. Numerous commercial interactions have supported data collection and analyses. In-kind support has also been provided by Sir Charles Gairdner Hospital, Cogstate Ltd., Hollywood Private Hospital, The University of Melbourne, and St Vincent’s Hospital. SR-S is supported by an NHMRC Investigator Grant (GNT1197315).

Supplementary Material

The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fnagi.2021.744872/full#supplementary-material

References

  1. Akash M. S., Rehman K., Chen S. (2014). Effects of coffee on type 2 diabetes mellitus. Nutrition 30 755–763. 10.1016/j.nut.2013.11.020 [DOI] [PubMed] [Google Scholar]
  2. Angulo E., Casado V., Mallol J., Canela E. I., Viñals F., Ferrer I., et al. (2003). A1 adenosine receptors accumulate in neurodegenerative structures in Alzheimer disease and mediate both amyloid precursor protein processing and tau phosphorylation and translocation. Brain Pathol. 13 440–451. 10.1111/j.1750-3639.2003.tb00475.x [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Arab L., Biggs M. L., O’Meara E. S., Longstreth W. T., Crane P. K., Fitzpatrick A. L. (2011). Gender differences in tea, coffee, and cognitive decline in the elderly: the cardiovascular health study. J. Alzheimers Dis. 27 553–566. 10.3233/jad-2011-110431 [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Araujo L. F., Mirza S. S., Bos D., Niessen W. J., Barreto S. M., van der Lugt A., et al. (2016). Association of coffee consumption with MRI markers and cognitive function: a population-based study. J. Alzheimers Dis. 53 451–461. 10.3233/jad-160116 [DOI] [PubMed] [Google Scholar]
  5. Arendash G. W., Schleif W., Rezai-Zadeh K., Jackson E. K., Zacharia L. C., Cracchiolo J. R., et al. (2006). Caffeine protects Alzheimer’s mice against cognitive impairment and reduces brain beta-amyloid production. Neuroscience 142 941–952. 10.1016/j.neuroscience.2006.07.021 [DOI] [PubMed] [Google Scholar]
  6. Basurto-Islas G., Blanchard J., Tung Y. C., Fernandez J. R., Voronkov M., Stock M., et al. (2014). Therapeutic benefits of a component of coffee in a rat model of Alzheimer’s disease. Neurobiol. Aging 35 2701–2712. 10.1016/j.neurobiolaging.2014.06.012 [DOI] [PMC free article] [PubMed] [Google Scholar]
  7. Boccardi M., Bocchetta M., Morency F. C., Collins D. L., Nishikawa M., Ganzola R., et al. (2015). Training labels for hippocampal segmentation based on the EADC-ADNI harmonized hippocampal protocol. Alzheimers Dement. 11 175–183. 10.1016/j.jalz.2014.12.002 [DOI] [PubMed] [Google Scholar]
  8. Boison D. (2006). Adenosine kinase, epilepsy and stroke: mechanisms and therapies. Trends Pharmacol. Sci. 27 652–658. 10.1016/j.tips.2006.10.008 [DOI] [PubMed] [Google Scholar]
  9. Bourgeat P., Dore V., Fripp J., Ames D., Masters C. L., Salvado O., et al. (2018). Implementing the centiloid transformation for (11)C-PiB and beta-amyloid (18)F-PET tracers using CapAIBL. Neuroimage 183 387–393. 10.1016/j.neuroimage.2018.08.044 [DOI] [PubMed] [Google Scholar]
  10. Bourgeat P., Dore V., Fripp J., Villemagne V. L., Rowe C. C., Salvado O. (2015). “Computational analysis of PET by AIBL (CapAIBL): a cloud-based processing pipeline for the quantification of PET images,” in Proceedings of the SPIE Medical Imaging 2015: Image Processing, Vol. 9413 (Orlando, FL: ). [Google Scholar]
  11. Chu Y. F., Chang W. H., Black R. M., Liu J. R., Sompol P., Chen Y., et al. (2012). Crude caffeine reduces memory impairment and amyloid beta(1-42) levels in an Alzheimer’s mouse model. Food Chem. 135 2095–2102. 10.1016/j.foodchem.2012.04.148 [DOI] [PubMed] [Google Scholar]
  12. de Paulis T., Schmidt D. E., Bruchey A. K., Kirby M. T., McDonald M. P., Commers P., et al. (2002). Dicinnamoylquinides in roasted coffee inhibit the human adenosine transporter. Eur. J. Pharmacol. 442 215–223. 10.1016/s0014-2999(02)01540-6 [DOI] [PubMed] [Google Scholar]
  13. Donohue M. C., Sperling R. A., Salmon D. P., Rentz D. M., Raman R., Thomas R. G., et al. (2014). The preclinical Alzheimer cognitive composite: measuring amyloid-related decline. JAMA Neurol. 71 961–970. 10.1001/jamaneurol.2014.803 [DOI] [PMC free article] [PubMed] [Google Scholar]
  14. Eskelinen M. H., Ngandu T., Tuomilehto J., Soininen H., Kivipelto M. (2009). Midlife coffee and tea drinking and the risk of late-life dementia: a population-based CAIDE study. J. Alzheimers Dis. 16 85–91. 10.3233/jad-2009-0920 [DOI] [PubMed] [Google Scholar]
  15. Fowler C., Rainey-Smith S. R., Bird S., Bomke J., Bourgeat P., Brown B. M., et al. (2021). Fifteen years of the australian imaging, biomarkers and lifestyle (AIBL) study: progress and observations from 2,359 older adults spanning the spectrum from cognitive normality to Alzheimer’s disease. J. Alzheimer’s Dis. Rep. 5 443–468. [DOI] [PMC free article] [PubMed] [Google Scholar]
  16. Gelber R. P., Petrovitch H., Masaki K. H., Ross G. W., White L. R. (2011). Coffee intake in midlife and risk of dementia and its neuropathologic correlates. J. Alzheimers Dis. 23 607–615. 10.3233/jad-2010-101428 [DOI] [PMC free article] [PubMed] [Google Scholar]
  17. Higgins L. G., Cavin C., Itoh K., Yamamoto M., Hayes J. D. (2008). Induction of cancer chemopreventive enzymes by coffee is mediated by transcription factor Nrf2. Evidence that the coffee-specific diterpenes cafestol and kahweol confer protection against acrolein. Toxicol. Appl. Pharmacol. 226 328–337. 10.1016/j.taap.2007.09.018 [DOI] [PubMed] [Google Scholar]
  18. Kim J. W., Byun M. S., Yi D., Lee J. H., Jeon S. Y., Jung G., et al. (2019). Coffee intake and decreased amyloid pathology in human brain. Transl. Psychiatry 9:270. [DOI] [PMC free article] [PubMed] [Google Scholar]
  19. Klunk W. E., Koeppe R. A., Price J. C., Benzinger T. L., Devous M. D., Jagust W. J., et al. (2015). The centiloid project: standardizing quantitative amyloid plaque estimation by PET. Alzheimers Dement. 11 1–15.e1-4. [DOI] [PMC free article] [PubMed] [Google Scholar]
  20. Laitala V. S., Kaprio J., Koskenvuo M., Raiha I., Rinne J. O., Silventoinen K. (2009). Coffee drinking in middle age is not associated with cognitive performance in old age. Am. J. Clin. Nutr. 90 640–646. 10.3945/ajcn.2009.27660 [DOI] [PubMed] [Google Scholar]
  21. Larsson S. C., Orsini N. (2011). Coffee consumption and risk of stroke: a dose-response meta-analysis of prospective studies. Am. J. Epidemiol. 174 993–1001. 10.1093/aje/kwr226 [DOI] [PubMed] [Google Scholar]
  22. Lassale C., Guilbert C., Keogh J., Syrette J., Lange K., Cox D. N. (2009). Estimating food intakes in Australia: validation of the commonwealth scientific and industrial research organisation (CSIRO) food frequency questionnaire against weighed dietary intakes. J. Hum. Nutr. Diet. 22 559–566. 10.1111/j.1365-277x.2009.00990.x [DOI] [PubMed] [Google Scholar]
  23. Liu Q. P., Wu Y. F., Cheng H. Y., Xia T., Ding H., Wang H., et al. (2016). Habitual coffee consumption and risk of cognitive decline/dementia: a systematic review and meta-analysis of prospective cohort studies. Nutrition 32 628–636. 10.1016/j.nut.2015.11.015 [DOI] [PubMed] [Google Scholar]
  24. Merighi S., Poloni T. E., Pelloni L., Pasquini S., Varani K., Vincenzi F., et al. (2021). An open question: is the A2A adenosine receptor a novel target for Alzheimer’s disease treatment? Front. Pharmacol. 12:652455. 10.3389/fphar.2021.652455 [DOI] [PMC free article] [PubMed] [Google Scholar]
  25. Mostofsky E., Rice M. S., Levitan E. B., Mittleman M. A. (2012). Habitual coffee consumption and risk of heart failure: a dose-response meta-analysis. Circ. Heart Fail. 5 401–405. 10.1161/circheartfailure.112.967299 [DOI] [PMC free article] [PubMed] [Google Scholar]
  26. Park H. M., Kim J. A., Kwak M. K. (2009). Protection against amyloid beta cytotoxicity by sulforaphane: role of the proteasome. Arch. Pharm. Res. 32 109–115. 10.1007/s12272-009-1124-2 [DOI] [PubMed] [Google Scholar]
  27. Perlaki G., Orsi G., Kovacs N., Schwarcz A., Pap Z., Kalmar Z., et al. (2011). Coffee consumption may influence hippocampal volume in young women. Brain Imaging Behav. 5 274–284. 10.1007/s11682-011-9131-6 [DOI] [PubMed] [Google Scholar]
  28. Prediger R. D., Batista L. C., Takahashi R. N. (2005). Caffeine reverses age-related deficits in olfactory discrimination and social recognition memory in rats. Involvement of adenosine A1 and A2A receptors. Neurobiol. Aging 26 957–964. 10.1016/j.neurobiolaging.2004.08.012 [DOI] [PubMed] [Google Scholar]
  29. Ross G. W., Abbott R. D., Petrovitch H., Morens D. M., Grandinetti A., Tung K. H., et al. (2000). Association of coffee and caffeine intake with the risk of Parkinson disease. JAMA 283 2674–2679. 10.1001/jama.283.20.2674 [DOI] [PubMed] [Google Scholar]
  30. Solfrizzi V., Panza F., Imbimbo B. P., D’Introno A., Galluzzo L., Gandin C., et al. (2015). Coffee consumption habits and the risk of mild cognitive impairment: the Italian longitudinal study on aging. J. Alzheimers Dis. 47 889–899. 10.3233/jad-150333 [DOI] [PubMed] [Google Scholar]
  31. Spiller M. A. (1984). The chemical components of coffee. Prog. Clin. Biol. Res. 158 91–147. [PubMed] [Google Scholar]
  32. van Gelder B. M., Buijsse B., Tijhuis M., Kalmijn S., Giampaoli S., Nissinen A., et al. (2007). Coffee consumption is inversely associated with cognitive decline in elderly European men: the FINE Study. Eur. J. Clin. Nutr. 61 226–232. 10.1038/sj.ejcn.1602495 [DOI] [PubMed] [Google Scholar]
  33. Van Leemput K., Maes F., Vandermeulen D., Suetens P. (1999). Automated model-based tissue classification of MR images of the brain. IEEE Trans. Med. Imaging 18 897–908. 10.1109/42.811270 [DOI] [PubMed] [Google Scholar]
  34. Villemagne V. L., Burnham S., Bourgeat P., Brown B., Ellis K. A., Salvado O., et al. (2013). Amyloid beta deposition, neurodegeneration, and cognitive decline in sporadic Alzheimer’s disease: a prospective cohort study. Lancet Neurol. 12 357–367. 10.1016/s1474-4422(13)70044-9 [DOI] [PubMed] [Google Scholar]
  35. Wang A., Wang S., Zhu C., Huang H., Wu L., Wan X., et al. (2016). Coffee and cancer risk: a meta-analysis of prospective observational studies. Sci. Rep. 6:33711. [DOI] [PMC free article] [PubMed] [Google Scholar]
  36. Wierzejska R. (2017). Can coffee consumption lower the risk of Alzheimer’s disease and Parkinson’s disease? A literature review. Arch. Med. Sci. 13 507–514. 10.5114/aoms.2016.63599 [DOI] [PMC free article] [PubMed] [Google Scholar]
  37. Wu L., Sun D., He Y. (2017). Coffee intake and the incident risk of cognitive disorders: a dose-response meta-analysis of nine prospective cohort studies. Clin. Nutr. 36 730–736. 10.1016/j.clnu.2016.05.015 [DOI] [PubMed] [Google Scholar]









Gerelateerde artikelen
 

Gerelateerde artikelen

Alcohol tast de darmbiotica >> ALDH4A1, een veel voorkomend >> Algemeen: Aangepast voedingspatroon >> Algemeen: Wat is er met ons >> Bloedverdunners die vitamine >> Boter vervangen door plantaardige >> Caffeine: mensen met een dieet >> Darmflora: Alzheimerpatiënten >> Darmflora beinvloed door voeding >> Deze 6 wetenschappelijke onderzoeken >>