Wie advies wilt over hoe het microbioom te verbeteren zou contact op kunnen nemen met deze website: Www.microbiome-Center.nl Voor zowel artsen als individuele burgers staat een groep van artsen en wetenschappers klaar om u een persoonlijk advies te geven.

Gerelateerd aan dit onderwerp is het wellicht interessant dit artikel in Kennislink  ook te lezen.

22 februari 2022: lees ook dit artikel: https://kanker-actueel.nl/NL/darmflora-beinvloed-door-voeding-en-leefstijl-speelt-cruciale-rol-in-ontstaan-van-ziektes-ook-bij-ontstaan-van-kanker-en-behandelingen-daarvan.html

Lees ook dit artikel over het darmmicrobioom en hoe je die kan testen: https://kanker-actueel.nl/NL/wat-is-een-darmmicrobioomtest-en-wat-zegt-een-uitslag-over-de-status-van-je-darmen-en-gezondheid-in-het-algemeen.html

22 februari 2022: VUmc Amsterdam

Uit recent Nederlands onderzoek blijkt dat patiënten met Alzheimer minder van een bepaald type bacteriën in hun darm hebben dan gezonde mensen. Die goede bacteriën worden vaak gezien bij mensen die veel vezels eten. Al eerder is aangetoond dat veel groente en fruit eten helpt tegen het ontstaan van dementie. Nu hebben onderzoekers van het VUmc ook daadwerkelijk aangetoond dat de darmflora - darmmicrobioom is gekoppeld aan Alzheimer. Al is nog niet duidelijk of Alzheimer ontstaat door een bepaalde darmflora - microbioom of andersom dat Alzheimer invloed heeft op de darmflora. 

Uit een AD artikel: Alzheimerpatiënten hebben vooral minder bacteriën van het soort dat zogenoemde korteketenvetzuren produceert. Van die vetzuren zoals boterzuur is al langer bekend dat ze een belangrijke rol spelen in het afweersysteem.

Wat we tot nu toe wisten over de relatie tussen het microbioom en alzheimer, kwam vooral uit dierproeven. Maar mensen zijn geen muizen, zegt Wiesje van der Flier, wetenschappelijk directeur van Alzheimercentrum Amsterdam van Amsterdam UMC. in een artikel in het Algemeen Dagblad. "Wel is er bij mensen eerder onderzoek gedaan naar het microbioom en de hersenen. Maar dat gaf nog geen inzicht in de relatie tussen darmbacteriën en alzheimerschade.”

"Bacteriën die stoffen als boterzuur produceren spelen ook een rol bij depressie”, zegt Robert Jan Brummer, MDL-arts en hoogleraar maag- darm- en leverziekten en klinische voeding. Duidelijk is alleen niet waar een depressie begint: in de darm of in de hersenen. Dat is voor Brummer ook niet interessant. ,,Als je de cirkel maar doorbreekt.”

Dat ligt voor alzheimer anders, zegt Van der Flier. ,,Een depressie kan weggaan en terugkomen. Alzheimer is een progressieve ziekte die nooit meer weggaat. ,,Daarom willen we weten of veranderingen in het microbioom tot alzheimer hersenschade leiden. Of veroorzaakt alzheimerhersenschade veranderingen in het microbioom?”

Het Algemeen Dagblad heeft dit artikel over de studie van het VUmc in de rubriek Koken en Weten: 

Alzheimerpatiënten missen goede bacterie in hun darmen, die gezonde mensen wel hebben

KOKEN & WETEN

In de rubriek Koken & Weten duikt gezondheidsjournalist Tijn Elferink in een voedingsonderwerp waar verwarring over bestaat. Dit keer: is er een dieet dat alzheimer kan voorkomen? 

Het is nog te kort door de bocht om te zeggen: ons eten heeft invloed op het ontstaan van de ziekte alzheimer. Maar uit nieuw Nederlands onderzoek blijkt wel dat patiënten met alzheimer minder van een bepaald type bacteriën in hun darm hebben dan gezonde mensen. Die bacteriën worden vaak gezien bij mensen die veel vezels eten. Niet voor niets dat al wel duidelijk is dat veel groente en fruit eten helpt tegen het ontstaan van dementie.>>>>>>>lees verder

Het studierapport van de onderzoekrs uit het VUmc is dit. Klik op de titel van het abstract voor het volledige verslag. 

ORIGINAL RESEARCH article

Front. Immunol., 31 January 2022 | https://doi.org/10.3389/fimmu.2021.794519

Gut Microbiota Composition Is Related to AD Pathology

Barbara J. H. Verhaar1,2,3*, Heleen M. A. Hendriksen3, Francisca A. de Leeuw3, Astrid S. Doorduijn3, Mardou van Leeuwenstijn3, Charlotte E. Teunissen4, Frederik Barkhof5,6, Philip Scheltens3, Robert Kraaij7, Cornelia M. van Duijn8,9, Max Nieuwdorp2, Majon Muller1 and Wiesje M. van der Flier3,10
  • 1Department of Internal Medicine - Geriatrics, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Center (UMC), Amsterdam, Netherlands
  • 2Department of Internal and Vascular Medicine, Amsterdam University Medical Center (UMC), Amsterdam, Netherlands
  • 3Alzheimer Center, Department of Neurology, Amsterdam Neuroscience, Amsterdam University Medical Center (UMC), Amsterdam, Netherlands
  • 4Department of Clinical Chemistry, Amsterdam University Medical Center (UMC), Amsterdam, Netherlands
  • 5Department of Radiology and Nuclear Medicine, Amsterdam University Medical Center (UMC), Amsterdam, Netherlands
  • 6University College London (UCL) Institutes of Neurology, Faculty of Brain Sciences, London, United Kingdom
  • 7Department of Internal Medicine, Erasmus Medical Center (MC), Rotterdam, Netherlands
  • 8Department of Epidemiology, Erasmus Medical Center (MC), Rotterdam, Netherlands
  • 9Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom
  • 10Department of Epidemiology and Data Science, Amsterdam University Medical Center (UMC), Vrije Universiteit Amsterdam, Amsterdam, Netherlands

Introduction: Several studies have reported alterations in gut microbiota composition of Alzheimer’s disease (AD) patients. However, the observed differences are not consistent across studies. We aimed to investigate associations between gut microbiota composition and AD biomarkers using machine learning models in patients with AD dementia, mild cognitive impairment (MCI) and subjective cognitive decline (SCD).

Materials and Methods: We included 170 patients from the Amsterdam Dementia Cohort, comprising 33 with AD dementia (66 ± 8 years, 46%F, mini-mental state examination (MMSE) 21[19-24]), 21 with MCI (64 ± 8 years, 43%F, MMSE 27[25-29]) and 116 with SCD (62 ± 8 years, 44%F, MMSE 29[28-30]). Fecal samples were collected and gut microbiome composition was determined using 16S rRNA sequencing. Biomarkers of AD included cerebrospinal fluid (CSF) amyloid-beta 1-42 (amyloid) and phosphorylated tau (p-tau), and MRI visual scores (medial temporal atrophy, global cortical atrophy, white matter hyperintensities). Associations between gut microbiota composition and dichotomized AD biomarkers were assessed with machine learning classification models. The two models with the highest area under the curve (AUC) were selected for logistic regression, to assess associations between the 20 best predicting microbes and the outcome measures from these machine learning models while adjusting for age, sex, BMI, diabetes, medication use, and MMSE.

Results: The machine learning prediction for amyloid and p-tau from microbiota composition performed best with AUCs of 0.64 and 0.63. Highest ranked microbes included several short chain fatty acid (SCFA)-producing species. Higher abundance of  leptum and lower abundance of  ventriosum group spp., Lachnospiraceae spp., Marvinbryantia spp., Monoglobus spp.,  torques group spp., Roseburia hominis, and Christensenellaceae R-7 spp., was associated with higher odds of amyloid positivity. We found associations between lower abundance of Lachnospiraceae spp., Lachnoclostridium spp., Roseburia hominis and Bilophila wadsworthia and higher odds of positive p-tau status.

Conclusions: Gut microbiota composition was associated with amyloid and p-tau status. We extend on recent studies that observed associations between SCFA levels and AD CSF biomarkers by showing that lower abundances of SCFA-producing microbes were associated with higher odds of positive amyloid and p-tau status.

Data Availability Statement

The datasets presented in this study can be found in online repositories. The names of the repository/repositories and accession number(s) can be found below: https://www.ebi.ac.uk/ena/browser/home, accession ID: PRJEB49329.

Ethics Statement

The studies involving human participants were reviewed and approved by Medisch Ethische Toetsingscommissie VUmc. The patients/participants provided their written informed consent to participate in this study.

Author Contributions

WF, CT, FB, PS, and CD contributed to conception and design of the study. HH, FL, AD, ML, and BV collected the data. RK was responsible for the sequencing of the samples. BV performed the statistical analyses. WF, MN, and MM contributed to the interpretation of the results. BV wrote the first draft of the manuscript. All authors contributed to manuscript revision, read, and approved the submitted version.

Funding

Research of Alzheimer Center Amsterdam is part of the neurodegeneration research program of Amsterdam Neuroscience. Alzheimer Center Amsterdam is supported by Stichting Alzheimer Nederland and Stichting VUmc fonds. The chair of WF is supported by the Pasman stichting. WF is recipient of a grant by Stichting Equilibrio and of ZonMW-Memorabel funded #733050814. The SCIENCe project is supported by a research grant of stichting Dioraphte. BV is appointed on an Amsterdam Cardiovascular Sciences (ACSPhD2019P003) and an Alzheimer Nederland grant (WE.03-2017-12). FB is supported by the NIHR biomedical research centre at UCLH. MN is supported by a personal ZONMW-VICI grant 2020 (09150182010020).

Conflict of Interest

CT received grants from the European Commission, the Dutch Research Council (ZonMW), Association of Frontotemporal Dementia/Alzheimer’s Drug Discovery Foundation, The Weston Brain Institute, Alzheimer Netherlands. CT has a collaboration contract with ADx Neurosciences, performed contract research or received grants from Probiodrug, Biogen, Esai, Toyama, Janssen prevention center, Boehringer, AxonNeurosciences, Fujirebio, EIP farma, PeopleBio, and Roche. FB is a consultant for Biogen-Idec, Bayer-Schering, Merck-Serono, Roche, Combinostics and IXICO; has received sponsorship from European Commission–Horizon 2020, National Institute for Health Research–University College London Hospitals Biomedical Research Centre, Novartis, and Merck; and serves on the editorial boards of Radiology, Neuroradiology, Multiple Sclerosis Journal, and Neurology. PS has received consultancy/speaker fees from Lilly, GE Healthcare, Novartis, Sanofi, Nutricia, Probiodrug, Biogen, Roche, Avraham, and EIP Pharma. PS has acquired grant support from GE Healthcare, Danone Research, Piramal, and MERCK. All funding was paid to the institution. MN is part of the Scientific Advisory Board of Caelus Health, The Netherlands and Kaleido Biosciences, USA. However, none of these are directly relevant to the current paper. WF received research funding from ZonMW, NWO, EU-FP7, EU-JPND, Alzheimer Nederland, CardioVascular Onderzoek Nederland, Health~Holland, Topsector Life Sciences & Health, stichting Dioraphte, Gieskes-Strijbis fonds, stichting Equilibrio, Pasman stichting, Biogen MA Inc, Boehringer Ingelheim, Life-MI, AVID, Roche BV, Fujifilm, Combinostics. WF holds the Pasman chair. WF is recipient of ABOARD, which is a public-private partnership receiving funding from ZonMW (#73305095007) and Health~Holland, Topsector Life Sciences & Health (PPP-allowance; #LSHM20106). She has performed contract research for Biogen MA Inc, and Boehringer Ingelheim. She has been an invited speaker at Boehringer Ingelheim, Biogen MA Inc, Danone, Eisai, WebMD Neurology (Medscape). WF is consultant to Oxford Health Policy Forum CIC, Roche, and Biogen MA Inc. WF participated in an advisory board of Biogen MA Inc and Roche. WF was associate editor of Alzheimer, Research & Therapy in 2020/2021. WF is associate editor at Brain. All funding was paid to the institution.

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.

Supplementary Material

The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fimmu.2021.794519/full#supplementary-material

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