Gut health and cognitive function -
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This study was supported by research grants from the Research Funding of Longevity Sciences 26—20, 27—21, 28—15, 30—1, and 19—24 , the National Center for Geriatrics and Gerontology, and the National Agriculture and Food Research Organization NARO Bio-oriented Technology Research Advancement Institution project Advanced Integration Research for Agriculture and Interdisciplinary Fields.
We thank Maki Yamamoto, Yukie Ohsaki, Saori Yoshimura, Hana Saito, and Ayaka Suzuki NCGG , and Yuya Shinkawa Kurume University for their technical and secretarial assistance, and the BioBank, NCGG, for quality control of the clinical samples and data.
We thank Rachel James and Lisa Giles, PhD, from Edanz Group www. Center for Comprehensive Care and Research on Memory Disorders, National Center for Geriatrics and Gerontology, Aichi, Japan.
Biostatistics Center, Graduate School of Medicine, Kurume University, Fukuoka, Japan. Laboratory of Food and Biomolecular Science, Department of Bioscience and Biotechnology for Future Bioindustries, Graduate School of Agricultural Science, Tohoku University, Miyagi, Japan. Medical Genome Center, National Center for Geriatrics and Gerontology, Aichi, Japan.
Department of Cognition and Behavioural Science, Nagoya University Graduate School of Medicine, Aichi, Japan. You can also search for this author in PubMed Google Scholar. is the principal investigator and contributed to the concept, drafting, and design of the protocol. and T.
Correspondence to Naoki Saji. have received research grants from the Research Funding of Longevity Sciences from the National Center for Geriatrics and Gerontology.
have received research funds for Comprehensive Research on Aging and Health from the Japan Agency for Medical Research and Development AMED. has received grants from the NARO Bio-oriented Technology Research Advancement Institution project Advanced Integration Research for Agriculture and Interdisciplinary Fields.
Open Access This article is licensed under a Creative Commons Attribution 4. Reprints and permissions. The relationship between the gut microbiome and mild cognitive impairment in patients without dementia: a cross-sectional study conducted in Japan.
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Subjects Dementia Microbiology Risk factors. Abstract Recent studies have revealed an association between the dysregulation of the gut microbiome and dementia. Introduction Mild cognitive impairment MCI refers to a very early stage of cognitive decline in patients not yet exhibiting dementia and is an important predictive risk factor for dementia 1.
Results Patient characteristics We previously analysed patients in the Gimlet study. Table 1 Demographics of the patients. Full size table. Table 2 Clinical findings of the patients. Table 3 Gut microbiome of the patients.
Table 4 Multivariable logistic regression analysis for the presence of MCI adjusted by enterotype I. Table 5 Multivariable logistic regression analysis for the presence of MCI adjusted by enterotype III.
Figure 1. Full size image. Discussion The primary finding of our present study was that the increased prevalence of Bacteroides , defined as enterotype I, was independently associated with the presence of MCI in patients without dementia. Conclusions We showed that components of the gut microbiome, in particular Bacteroides , may be associated with the presence of MCI in patients without dementia.
Methods Study design This study was a sub-analysis of our previously published, single-centre observational study Gimlet study 5. Brain imaging Patients underwent a 1. References Livingston, G. Article PubMed Google Scholar Ganguli, M. Article PubMed PubMed Central Google Scholar Saji, N.
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Article CAS PubMed PubMed Central Google Scholar Spychala, M. Article CAS PubMed PubMed Central Google Scholar Download references. Acknowledgements This study was supported by research grants from the Research Funding of Longevity Sciences 26—20, 27—21, 28—15, 30—1, and 19—24 , the National Center for Geriatrics and Gerontology, and the National Agriculture and Food Research Organization NARO Bio-oriented Technology Research Advancement Institution project Advanced Integration Research for Agriculture and Interdisciplinary Fields.
View author publications. Ethics declarations Competing interests N. Supplementary information. Rights and permissions Open Access This article is licensed under a Creative Commons Attribution 4. About this article. Cite this article Saji, N. Copy to clipboard. Heston Kendra L. Hanslik Tyler K. Ulland Scientific Reports Comments By submitting a comment you agree to abide by our Terms and Community Guidelines.
About the journal Open Access Fees and Funding About Scientific Reports Contact Journal policies Calls for Papers Guide to referees Editor's Choice Journal highlights. Research in the past decade has found that gut bacteria may influence our emotions and cognitive capabilities.
For example, some bacteria make oxytocin, a hormone our own bodies produce that encourages increased social behavior. Other bacteria make substances that cause symptoms of depression and anxiety. Still others make substances that help us to be calmer under stress.
Yes, I know: I want some more of those bacteria, too. Finally, the gut bacteria also have been shown to influence our vulnerability to certain brain diseases, including Alzheimer's disease, Parkinson's disease, and autism. For example, a substance called synuclein, found in the brains of people with Parkinson's disease, is made by gut bacteria and can travel via nerves from the gut to the brain.
Recognizing the roles that the bacteria and viruses and other microbes inside us appear to play in our health, even in our personality, has been one of the most important discoveries of the past 50 years.
Conversely, the Mediterranean MED diet, which emphasizes increased intake of nonrefined grains, fruits and vegetables, legumes, nuts, fish, and lower intake of red meat and processed foods, is associated with improved cognition and reduced dementia risk The MED diet benefits the brain by reducing inflammation and oxidative stress 25 , promoting neurogenesis, and improving neuronal connectivity Furthermore, contrary to the Western diet, the MED diet is associated with improved gut microbiome composition and diversity and decreased gut permeability and inflammation The MED diet is high in fermentable dietary fibers and is associated with enhanced abundance of fiber-fermenting bacteria leading to increased SCFAs in the gut and bloodstream In addition to promoting gut health, SCFAs play a role in maintaining the blood—brain barrier 29 and exhibit neuroactive properties such as support of glial cells 30 and modulation of neurotrophic factors Altered SCFA production has been demonstrated in a variety of neuropathologies, including AD Another key feature of the MED diet is omega-3 polyunsaturated fatty acids PUFAs found in fatty fish eicosapentaenoic acid and docosahexaenoic acid and derived from alpha-linolenic acid found in nuts, seeds, legumes, and green leafy vegetables The intake of omega-3 PUFAs correlates with improved microbiome composition and diversity and increased SCFA-producing bacteria Omega-3 PUFAs are essential in maintaining gut epithelial integrity 35 and act as intra- and intercellular signaling mediators in the GI tract and brain, influencing immune regulation, inflammation, and homeostasis Polyphenols found in plant foods such as fruits, vegetables, herbs, and wine are abundant in the MED diet and promote beneficial bacteria in the gut 37 , When processed by gut microbiota, they increase the bioavailability of polyphenol-derived metabolites, which protect against neurotoxic injury, suppress inflammation, and promote cognitive functions 39 , The majority of diet interventions measuring both microbiome and cognitive outcomes have been conducted in rodents and have investigated individual components of Western and MED diets.
One human study has investigated the impact of a MED diet on the gut microbiome and cognition in older adults.
The following is a review of the intervention literature. Diets high in saturated fat are the most commonly studied interventions associated with a Western eating pattern Supplementary Table S1. They appear to consistently alter microbiota, but simultaneous cognitive changes are not always observed.
HFD yielded a greater relative abundance of genera from Firmicutes phylum and lower abundance of genera from Bacteroidetes phylum. Microglial characterization and counts in the cortex, hippocampus, and hypothalamus did not identify differences in neuroinflammation between groups.
Bacteria from Lachnospiraceae and Ruminococcace families were correlated with memory. No differences in neuroinflammation or brain-derived neurotrophic factor BDNF expression were observed. Associations were observed between altered taxa and cognitive flexibility.
HFD increased Proteobacteria population, increased fecal and plasma LPS, and suppressed BDNF expression in the hippocampus. Inconsistent findings may be due to variations in rodent age, strain, and diet composition.
For instance, some studies did not match for caloric value, fiber, sucrose, or protein content In HFD interventions with calorie-matched designs 41 , 42 , HFD groups eat less food overall compared with controls and are less exposed to certain nutrients eg, sucrose.
Other studies substituted fat calories with sucrose in control diets 44 , Thus, the negative effects of HFD may be offset by negative effects of sucrose. Rodents fed detrimental diets for prolonged periods will develop various cardiometabolic impairments, making it difficult to directly link diet to microbiota and cognition.
To address this, Bruce-Keller et al. HFD transplantation altered microbiota diversity and composition mainly shifts of Firmicutes phylum and led to greater intestinal inflammation and permeability. Memory performance was significantly lower in HFD recipient mice who also showed neuroinflammation and disrupted cerebrovascular homeostasis in the medial prefrontal cortex.
Diets high in sucrose appear to consistently affect gut microbiota and cognition. HSD increased bacteria from Clostridiales and Lactobacilllales orders and decreased bacteria from Bacteroidales order. Altered taxa were related to poorer cognitive flexibility; however, the diets in this study were not nutrient matched, which makes it difficult to determine which nutrients are responsible for differences between groups.
Bacteria from Lachnospiraceae and Ruminococcace families were correlated with memory, but no differences in neuroinflammation or BDNF expression were observed. The HSD group displayed increases in bacteria from Lachnospiraceae and Ruminococcace families, and decreased BDNF expression and genes regulating catecholamine metabolism in the prefrontal cortex.
The cafeteria diet is an experimental rodent diet of unhealthy human foods, which are highly processed and high in saturated fat and sucrose. Both diets increased hippocampal cytokine expression, but only the continuous cafeteria diet was associated with impaired short-term memory.
Limited access to unhealthy foods may spare cognition, as intermittent caloric restriction has shown to improve cognition in mice Genes related to neuroinflammation and neurotransmission in adulthood were also affected. In this study, mice were switched back to a normal chow diet following adolescence.
Switching to a chow diet after HFD intervention has shown to reverse behavioral effects 53 , which may explain the lack of cognitive differences in adulthood. The foods typical in a MED diet are high in fiber.
β-Glucans, soluble fibers found in fungi, yeast, and cereal grains such as oats and barley, have shown to alter microbiota and cognition in several rodent models Supplementary Table S2.
Increases in hippocampal SCFAs and reductions in neuroinflammation and brain insulin resistance were also observed. Oat-derived β-glucan also countered HFD-induced upregulation of inflammatory cytokines in the hippocampus and decreased endotoxin translocation in the colon.
A substudy of these mice found that microbiota changes preceded cognitive changes, and cognitive effects of β-glucan were eliminated in an additional study arm receiving antibiotics in combination with the oat β-glucan diet.
Similar effects of β-glucan-rich foods have been observed. Oat fiber ameliorated impairments in spatial learning and memory, and improved microbiota diversity, increasing SCFA-producing microbiota increased Actinobacteria and decreased Rikenellaceae.
Oat fiber also increased the expression of SCFA receptors and tight junction proteins in the distal colon. Barley, a β-glucan-rich food, has shown to ameliorate cognitive impairments and alter gut microbiota in a rodent model of age-related cognitive decline The barley diet altered microbiota increased Bacteroides to Firmicutes ratio and reduced age-associated spatial memory decline compared with the rice diet.
Microbiota-accessible carbohydrates MAC are supplements rich in a variety of fermentable fibers. MAC effects on cognition were eliminated when combined with antibiotics in an additional study arm.
Purified fiber supplementation has shown to alter microbiota and cognition in a small sample of healthy young adult females. Participants received either PDX resulted in modest cognitive improvements and compositional microbiota changes increased relative abundance of Firmicutes.
Minor changes to CD62L receptor expression, a marker of acute stress responsiveness, suggest that PDX benefits the brain by reducing inflammatory status.
PDX, however, is a synthetic polymer, not naturally found in foods and may not represent the effects of fiber as part of a MED diet. PUFA-enriched diet interventions positively affect gut microbiota, with simultaneous cognitive effects most often observed.
In stress-induced adolescent male Wistar rats, a diet enriched in omega-3 PUFAs prevented memory impairments, normalized declines in hippocampal BDNF, and attenuated shifts in microbial composition increased relative abundance of Ruminococcacea and Lachnospiraceae compared with a control diet These effects were maintained throughout adulthood, long after the stressful environment was terminated.
Behavioral changes were closely associated with alterations in gut microbiota. In contrast, 2 weeks of a PUFA-enriched diet in adolescent male Sprague Dawley rats led to significant differences in microbiota composition specifically taxa from Ruminococcaceae family , but not object or recognition memory compared with controls Sesamol, a polyphenol derived from sesame oil, has shown to alter microbiota while also reducing age-associated impairments in mice Young 2 months old and middle-aged 12 months CD-1 male mice on a standard chow diet AINM were compared with middle-aged male mice on a chow diet with sesamol 0.
Sesamol reduced cognitive impairments observed in aging mice on a chow-only diet and significantly increased microbiota diversity, with beneficial effects seen on aging- and inflammation-associated microbiota. Oxidative stress and neuroinflammation were significantly reduced compared with controls, likely related to alleviated intestinal barrier damage and inhibited gut microbiome-driven LPS entry into the blood.
The NU-AGE study new dietary strategies addressing the specific needs of the older adult population for healthy aging in Europe is the only whole diet intervention in humans that has reported on measures of both gut microbiota and cognition.
A sample of older adults aged 65—79 years were randomized to either a MED diet intervention or control diet for 12 months Participants with high MED diet adherence showed significant improvements in global cognition and episodic memory. Gut microbial communities were profiled in a subset of participants on MED diet, controls.
There were no significant differences in microbiota diversity between groups; however, across all participants, greater MED diet adherence was associated with increased microbiome diversity, increased SCFAs, and decreased inflammation Bacterial communities enriched by the MED diet were positively associated with memory and visual-spatial abilities.
Most exercise examined in the context of the microbiome describes aerobic exercise. Aerobic exercise throughout the life span is associated with better cognitive function and reduced dementia risk It is proposed to benefit the brain both indirectly, by improving health conditions, and directly, by increasing brain neurotrophic factors, improving cerebrovascular function, and enhancing brain plasticity 64— Exercise also increases key antioxidant enzymes, anti-inflammatory cytokines, and antiapoptotic proteins, leading to reduced inflammation 67 , Aerobic exercise improves microbial diversity and intestinal barrier permeability in humans 20 , 69 , BDNF is elevated by exercise and has shown to regulate GI tight junction proteins, which are crucial for maintaining the epithelial integrity, thereby reducing the translocation of proinflammatory endotoxins eg, LPS into circulation Greater exercise and cardiorespiratory fitness are positively associated with SCFA-producing bacteria and fecal SCFA concentrations independent of diet 72 , The effects of aerobic exercise on gut health appear to vary by exercise intensity.
Moderate-intensity aerobic exercise maintains intestinal blood flow, positively modulating GI motility 74 and reducing inflammation High-intensity interval training, which involves short-duration bursts of strenuous aerobic exercise, has shown to beneficially alter microbiota composition and diversity in mice 80—82 and reduce systemic and adipocyte inflammation in rats A better understanding of the effects of varying types and intensities of exercise on the gut—brain axis in humans is required.
Very few exercise interventions rodent only met the criteria for inclusion in this review. Aerobic exercise interventions alter gut microbiota and positively influence brain health in rodents, but evidence in humans is unexplored Supplementary Table S3.
Memory performance was associated with bacterial abundances from Ruminococcaceae and Lachnospiraceae families.
In a rat model of metabolic syndrome, preoperative treadmill exercise increased microbiome diversity increased abundance of Firmicutes and decreased abundance of Bacteroidetes and alleviated postoperative cognitive impairments 84 , a common issue in older adult patients with metabolic syndrome.
Male high- and low-capacity running rats were randomly assigned to receive preoperative exercise 6 weeks with surgery tibia fracture with internal fixation under anesthesia or sham surgery anesthesia only , or no exercise with surgery or sham surgery. Preoperative exercise attenuated memory impairments and lowered neuroinflammation in low-capacity running rats postsurgery.
Exercise increased the abundance of SCFA-producing bacteria and elevated levels of Lactobacillus reuteri, a vitamin B 12 producer.
No differences in spatial memory were observed, but the exercise group showed decreases in the size and number of beta-amyloid plaques in the hippocampus. The findings mostly from rodent trials provide evidence for the mediating effect of gut microbiota on diet and exercise effects on cognition Figure 1.
Western-type diets were associated with decreased microbiota richness and diversity 45 , 51 and poorer spatial and object recognition memory 42 , 43 , 46 , 47 , 49—51 , as well as increased intestinal and neural inflammation 45—47 , 49 , 51 , and decreased BDNF expression Interventions associated with MED eating patterns often resulted in greater microbiota diversity 46 , 60 , 62 and spatial and object recognition memory 54— Following a MED diet intervention in older adults, correlations between diet-associated microbiota changes and global cognition were observed Increased SCFAs and tight junction proteins 45 , 54 , 55 , 62 , hippocampal BDNF expression 58 and reduced endotoxin translocation 45 , 46 , 60 , brain insulin resistance 54 , and neuroinflammation 45 , 54 , 60 , 62 were identified as potential mediating mechanisms in these studies.
Not all diet interventions observed cognitive effects however, and these inconsistencies are likely due to heterogeneity of diets, rodent models, and cognitive assessments.
The most promising evidence comes from high-fiber interventions where increased SCFAs and reduced inflammation along with cognitive changes were commonly observed 45 , 46 , 54— Summary of intervention results. Dashed arrows denote mixed evidence for cognitive effects. Evidence from a limited number of preclinical exercise trials have shown compositional microbiota changes that were associated with cognition in healthy mice 44 and reduced postoperative cognitive impairment and neuroinflammation in a rat model of metabolic syndrome In AD mice, high-intensity treadmill exercise led to increases in SCFA-producing bacteria and reductions in AD pathology 80 , but not cognitive differences.
The lack of cognitive effects in AD mice may be related to their advanced disease progression and aligns with the notion that interventions should be applied early in the course of cognitive decline Supporting the mediating the role of the microbiome are microbiota changes that precede cognitive changes 45 , antibiotic elimination of cognitive effects related to diet 45 , 46 , microbiota transplant effects 49 , and potential mechanistic links such as SCFA, BDNF, and inflammatory changes.
Associations between altered microbiota and cognition were also frequently observed 42—44 , 51 , 54 , 59 , In particular, bacteria from the Clostridia class and Bacteroidales order, such as Lachnospiraceae, Ruminococcaceae, Coprobacter, and Rikenella, as well as Lactobacillus and Bifidobacterium genera.
The field is predominantly dominated by rodent studies, but their findings set the stage for future human trials in this area. Several ongoing human studies are described in the following section. Participants will be randomly assigned to one of the following groups: MED diet to maintain body weight; MED diet to achieve weight loss; typical American diet to achieve weight loss.
The 3-group design could give insight on whether the MED diet affects microbiome and cognition independent of adiposity and metabolic changes. The COMBAT study 87 will investigate the impact of 12 weeks of cranberry intake, rich in polyphenols, on gut microbiota and cognition.
Blood, urine, and fecal samples will be collected to assess diet and microbiome, and all participants will undergo cognitive testing and magnetic resonance imaging MRI. Secondary analyses of inflammatory and metabolic markers, BDNF levels, and cerebrovascular hemodynamics will be conducted.
Strengths of this study include the recruitment of older adults and a comprehensive brain health assessment. The use of a single nutrient intervention, however, only informs us about one attribute of a healthy diet.
The intervention will consist of a low-fat vegan diet, aerobic and resistance exercise, stress management, and group support.
A waitlist control group will be used, and after 20 weeks, those in the control phase will receive the lifestyle intervention. Cognition and microbiome changes will be assessed at 20 and 40 weeks.
The intervention design limits the ability to assess individual lifestyle components and may only be able to inform on the overall combined effects of the intervention. A study from Sun Yat-sen University in China 89 aims to examine the effects of a combined diet and exercise intervention versus either intervention alone on executive function and intestinal microbiota in undergraduate students.
Exercise training will consist of rope skipping 3 cycles of 20 minutes skipping: minute breaks 3 times per week. The diet intervention consists of 10 hours of restricted eating of a high-fiber diet.
Secondary outcomes will include BDNF, CRP, and a variety of inflammatory cytokines. Limitations of this study include the young study sample, lack of a true control group, and the assessment of only one cognitive domain. Additionally, restricted eating does not necessarily reflect a healthy diet, and rope skipping for long durations does not seem appropriate for adults without a moderate fitness level at baseline.
The aforementioned studies speak to the growing interest in the effects of lifestyle modification on the gut—brain axis, but are limited by various sample populations, intervention protocols, and outcome measures. Strengths of these studies include the study of at-risk populations, high-intensity exercise, and multicomponent intervention effects.
They also provide a sense of appropriate designs and outcome measures. There are still, however, many gaps in the field that need to be addressed. The role of the microbiome in the effects of diet and exercise on cognition is emerging from preclinical trials, but inferences to human physiology, especially in the context of dementia prevention, are uncertain Figure 2.
A major limitation of rodent research is the narrow selection of cognitive tests. Spatial and object recognition are most always reported due to the frequent use of maze testing and fear conditioning paradigms.
Thus, little is known about other cognitive domains, which can be differently impaired in humans experiencing dementia. Human trials provide the opportunity to comprehensively study cognition through neuropsychological assessment and the use of advanced measurement techniques such as MRI.
There are numerous studies investigating the effects of diet and exercise on cognition in older adults, but lacking investigation into the microbiome. We encourage researchers working on these studies to collaborate with microbiome scientists, and attempt to include simple, cost-effective measures of microbiota composition, diversity, and function.
The majority of studies investigated singular components of Western and MED eating patterns, and the effects of whole diet interventions on microbiota and cognition are underexplored. High-fat and high-sucrose diets are common in North America; thus, there is a lot of research interest in their effects.
Furthermore, the frequent use of single nutrient interventions may reflect the desire to discover simple forms of treatment.
The general consensus, however, is that the combined attributes of a diet are more important for microbiome composition and cognition than individual components Nutrients that target SCFA-producing bacteria and inflammation appear to have the greatest impact on cognition.
Thus, whole diets such as the MED diet, which comprised fruits, vegetables, and healthy fats, are recommended for future studies. The number of exercise interventions in this field is quite limited compared with dietary interventions. Additional preclinical trials are needed to corroborate the current evidence from a handful of rodent studies and inform the designs of human trials.
Little is known about how exercise intensity influences the gut—brain axis, and thus is an important endeavor for future research, as differing intensities have shown to have varying effects on gut health and other physiological outcomes 77— Researchers should also consider investigating other types of exercise, such as resistance training.
Microbiota transplant and antibiotic treatment designs should also be considered in rodent exercise studies. None of the reviewed exercise interventions measured BDNF, but given that BDNF is elevated by exercise and associated with gut health and cognition, it is recommended that future exercise trials include this as an outcome.
The diet interventions included in this study could warrant their own review entirely; however, it was our intent to present findings from both diet and exercise interventions as there is accruing evidence supporting the synergistic effects of multicomponent lifestyle interventions, and it is of interest whether these are replicated when assessing microbiome and cognitive outcomes 90 , Diet and exercise-associated microbiome and cognitive changes are accompanied by many of the same physiological changes; thus, it is reasonable to predict that synergistic effects may occur.
Factorial designs comparing diet, exercise, and diet combined with exercise are highly encouraged to tease apart these relationships. The majority of studies reviewed included heterogeneous, mostly male rodent models. Findings from adolescent, young adult, and stress-induced mice may not generalize to at-risk populations, while, conversely, AD rodent models may be too far along in their disease progression.
Most studies used healthy adult rodents, a group of interest considering many risk factors for dementia begin early in adult life, and lifestyle behaviors during adulthood are associated with cognition in late life Findings from studies including middle-aged, senescence-accelerated, and cardiometabolic risk rodent models are perhaps the most relevant to dementia prevention and are recommended for future studies.
Researchers also tend to use male mice exclusively as they are concerned that estrous cycles in female mice will increase variability; however, these claims have been refuted The underrepresentation of female rodents limits our understanding of female biology and may lead to inadequate treatment for females.
Given there are sex and gender differences in cognitive trajectories 94 and lifestyle preferences 95 , 96 , it is important to study the effects of diet and exercise on the gut—brain axis as a function of both sex and gender.
Despite these limitations, we believe that for a research area still in its infancy, it is appropriate to consider findings from all studies available that investigate the interplay between diet, exercise, and the gut—brain axis.
Lastly, a major focus of this review was to infer the mediating role of the microbiome; however, no studies conducted proper mediation analyses. Instead, our conclusions are drawn from evidence of potential mediating mechanisms, correlations between altered microbiota and cognition, and novel designs such as microbiota transplant and antibiotic treatment.
Most studies did not assess microbiota and cognition at baseline, a requirement for running proper mediation analyses. Figure 3 provides an example of a trial design for future exercise and diet investigating the mediating role of the gut microbiome on cognitive changes in older adults.
In addition to baseline and postintervention assessments, midpoint assessments are useful for identifying whether microbiota changes precede cognitive changes. Measuring potential mediating mechanisms such as SCFAs and tight junction proteins, BDNF, and measures of local, systemic, and neural inflammation are highly recommended.
Suggested trial design. The intervention literature supports the notion that the gut microbiome, at least in part, mediates diet and exercise effects on cognition. In contrast to Western-style diets, interventions encompassing features of the MED diet, and uptake of exercise were associated with improved microbiota diversity, increased SCFA production, and reduced local and systemic inflammation.
The evidence is mainly derived from rodent studies; however, one large MED diet intervention found diet-associated microbiota changes to be correlated with cognitive performance in older adults. Several diet and exercise interventions assessing both microbiome and cognitive outcomes in humans are underway, but are limited by heterogeneous populations and interventions.
We encourage the inclusion of baseline and follow-up measures of microbiome composition, diversity, and function in lifestyle interventions aimed at reducing dementia risk in older adults. This effort would help to elucidate the mechanisms by which lifestyle modification affects cognition and may help to develop more targeted dementia prevention strategies.
This work was supported by a grant from the Canadian Consortium on Neurodegeneration in Aging CCNA , which is supported by the Canadian Institutes of Health Research CIHR with funding from several partners.
The salary of N. was supported by the grant. The sponsors are not involved in the preparation of the paper. Everyone who has significantly contributed to this work has been listed as coauthor. participated in the conceptualization of the project.
aggregated the data and was the lead writer of the original draft. supported the writing of the original draft. All coauthors were equally involved in reviewing, editing, and approving the final version of this manuscript.
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Translational Neurodegeneration volume 11Article cognktive 49 Runction this article. Metrics details. Guut axis may be involved functionn the progression cohnitive age-related cognitive impairment and relevant brain structure cognitve, but evidence from large Gut health and cognitive function cohorts Muscle definition vs lacking. This study was aimed to investigate the associations of gut microbiome with cognitive impairment and brain structure based on multi-omics from three independent populations. We included participants from the Guangzhou Nutrition and Health Study GNHS with both gut microbiome and cognitive assessment data available as a discovery cohort, of whom individuals provided fecal samples twice before cognitive assessment. We selected individuals with baseline microbiome data for brain magnetic resonance imaging during the follow-up visit.Gut health and cognitive function -
Scientists are discovering many ways in which the microorganisms living in the human gastrointestinal tract can influence health. These organisms — collectively called the microbiome — are incredibly diverse, and there has been an explosion of research studies investigating this fascinating link over the past few years.
Previous studies in animal experiments and small clinical studies have shown changes in cognition might link to changes in the gut microbiome. However, few studies have investigated gut microbiota and cognition in large samples from community settings.
Researchers from the United States have recently analyzed data from a large cross-sectional study and found a link between gut microbial composition and cognitive status in middle-aged adults.
The participants were recruited from four centers across the U. as part of the CARDIA — Coronary Artery Risk Development in Young Adults — study. These findings add to a growing body of literature suggesting that gut microbiota may be associated with cognitive aging.
The results appear in JAMA Neurology. Michelle Wright, Ph. Many of these factors have been studied independently, and in animal models, but this study evaluated many of these features together, for the first time among a community-dwelling sample, using existing data.
The study team decided to use data that had already been collected for the CARDIA study. CARDIA is a population-based study of Black and white adults living in four urban areas: Chicago, Minneapolis, Birmingham, AL, and Oakland, CA.
All participants were offered a set of cognitive assessments as part of the study, with 3, completing at least one assessment. In addition, of these participants were recruited into a microbiome sub-study that sent stool samples to a central laboratory for DNA sequencing.
The participants completed six cognitive tests: the Digit Symbol Substitution Test DSST , Rey-Auditory Verbal Learning Test, the timed Stroop test, letter fluency, category fluency, and the Montreal Cognitive Assessment. The researchers accounted for other factors that might influence either test scores or the microbiome composition in their analysis.
The researchers also collected data on comorbidities, such as hypertension and diabetes. Of the participants who signed up for the microbiome study, had stool samples suitable for DNA sequencing. Ten participants did not have complete data on the cognitive tests, meaning the analysis used data from people.
Participants were 48—60 years old, with a mean age of 55 — The analysis focused on three areas: between-person diversity, within-person diversity, and the individual composition of microorganisms in the stool samples.
Looking at the between-person differences, microbial composition was significantly associated with cognitive measures when adjusted for the risk factors.
The team observed a statistically significant interaction by sex, and there was no significant difference in race. In contrast, within-person microbial diversity was generally not associated with cognition in these data. Once the results had been fully adjusted for any confounding factors, the genera Barnesiella , Lachnospiraceae , and Akkermansia were positively associated with at least one of the cognitive tests.
Sutterella was negatively associated with the Montreal Cognitive Assessment test. One mechanism that might help explain these results could be the production of short-chain fatty acids. These are one of the main byproducts of the microbiome and may have neuroactive properties.
Scientists believe that short-chain fatty acids play a part in regulating how the gut and brain interact, that is, the gut-brain axis. In animal studies, short-chain fatty acids appear to be protective against vascular dementia and cognitive impairment.
Brenda Wilson, Ph. The authors of the paper acknowledge that their sample size is quite small, especially when using it for multiple comparisons.
Measuring gut microbiota from a single stool sample would not capture between-person differences consistently, as the composition might change — although the team says that studies of U. populations have noted relative stability over 6—12 months. Also, because samples were taken at a single time point, changes in health that might cause shifts in the microbial community are not captured in the data.
Finally, the type of analysis used to sequence the DNA yields results about the composition, but not necessarily the function of the microbiome. They add that data collected over multiple time points is needed. This could confirm that gut microbial changes occur before the physiological changes.
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PLoS ONE. Naugle RIKK. Limitations of the Mini-Mental State Examination. Cleve Clin J Med. Download references. We thank all the participants involved in the three populations and Westlake University Supercomputer Center for the assistance in data storage and computation.
We thank the support from Westlake Education Foundation and Westlake Intelligent Biomarker Discovery Lab at the Westlake Laboratory of Life Sciences and Biomedicine.
This study was funded by the National Natural Science Foundation of China , , , and , Zhejiang Ten-thousand Talents Program R , and Zhejiang Provincial Natural Science Foundation of China LQ21H CHNS received funding from the National Institutes of Health NIH R01HD, R01AG, P30DK, and R01HD from to and was supported by the National Institutes of Health and National Institute of Diabetes and Digestive and Kidney Diseases R01DK and the Carolina Population Center P2CHD, P30AG The funders had no role in collecting data, study design, interpretation of data or the decision to submit the manuscript for publication.
College of Life Sciences, Zhejiang University, Hangzhou, , China. School of Life Sciences, Westlake University, 18 Shilongshan Rd, Cloud Town, Hangzhou, , China. Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Department of Medical Statistics and Epidemiology, School of Public Health, Sun Yat-Sen University, Guangzhou, , China.
Chinese Center for Disease Control and Prevention, National Institute for Nutrition and Health, Beijing, , China. School of Public Health, Hainan Medical University, Haikou, , China. Westlake Intelligent Biomarker Discovery Lab, Westlake Laboratory of Life Sciences and Biomedicine, Hangzhou, , China.
Department of Neurology and Institute of Neurology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, , China. Key Laboratory of Trace Element Nutrition, National Health Commission, Beijing, , China.
Institute of Basic Medical Sciences, Westlake Institute for Advanced Study, Hangzhou, , China. You can also search for this author in PubMed Google Scholar.
JSZ, YMC, BZ and SDC conceived the study concept and design. WTC, ZHW, XFJ, CYL, HRL, HLZ, and SDC collected the data. ZLM, WLG, and MLS processed the biological samples. ZLJ, KZ, YJH, and XXL supported microbial and imaging data for analysis.
XXL and YQF did the statistical analysis. XXL, YQF, and JSZ wrote the manuscript. All authors critically reviewed the article and approved the final manuscript. Correspondence to Shengdi Chen , Bing Zhang , Yu-ming Chen or Ju-Sheng Zheng.
The GNHS study protocol was approved by the Ethics Committee of the School of Public Health at Sun Yat-sen University and the Ethics Committee of Westlake University.
The study protocol of CHNS was approved by the Institutional Review Boards of the Chinese Center for Disease Control and Prevention, University of North Carolina at Chapel Hill and the National Institute for Nutrition and Health.
Informed consents were obtained from all participants. Table S1. Participant characteristics in the GNHS. Table S2. Participant characteristics of the CHNS. Table S3. Table S4. Table S5. Weights for genus features contributing to the LASSO models.
Table S6. Table S7. Associations between Odoribacter and SCFAs in the GNHS. Table S8. Associations between serum acetic acid and brain structure in the GNHS.
Table S9. Distribution of metagenomic features in the GNHS. Table S Associations between intra-individual alterations in gut microbial composition and cognitive impairment in the GNHS. Metagenomic and metabolomic features associated with cognitive impairment in the GNHS.
Correlations of metagenomic and metabolic features with MMSE domains in the GNHS. Correlations between metagenomic features and metabolites in the GNHS. S1 Overview of the multi-omics datasets of the GNHS. S2 Distribution of metagenomic and metabolomic features in the GNHS.
S3 Correlation analyses on cognition-related metagenomic and metabolic traits in the GNHS. S4 Association of metagenomic pathways and serum metabolomics with cognitive function in the GNHS.
S5 Networks of metagenomic pathways in the GNHS. Open Access This article is licensed under a Creative Commons Attribution 4. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material.
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Reprints and permissions. Liang, X. et al. Gut microbiome, cognitive function and brain structure: a multi-omics integration analysis. Transl Neurodegener 11 , 49 Download citation. Received : 30 May Accepted : 01 November Published : 14 November Anyone you share the following link with will be able to read this content:.
Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search all BMC articles Search. Download PDF. Abstract Background Microbiome-gut-brain axis may be involved in the progression of age-related cognitive impairment and relevant brain structure changes, but evidence from large human cohorts is lacking.
Methods We included participants from the Guangzhou Nutrition and Health Study GNHS with both gut microbiome and cognitive assessment data available as a discovery cohort, of whom individuals provided fecal samples twice before cognitive assessment.
Results We found protective associations of specific gut microbial genera Odoribacter , Butyricimonas , and Bacteroides with cognitive impairment in both the discovery cohort and the replication study 1.
Conclusions Our findings reveal that specific gut microbial features are closely associated with cognitive impairment and decreased hippocampal volume, which may play an important role in dementia development.
Background The number of elderly people living with dementia is rising especially in low- and middle-income countries [ 1 ]. Methods Study populations and design Discovery cohort The main analyses were based on the Guangzhou Nutrition and Health Study GNHS , a community-based prospective cohort study in southern China.
Replication studies To validate the results discovered with cognitive scores, we performed the same analysis in an AD case—control study replication study 1; 30 AD patients, 30 MCI patients, and 30 healthy controls which was published recently [ 8 ]. Cognitive assessment The MMSE, established by Folstein in [ 14 ], is one of the most widely used instruments for cognitive screening in clinical settings and epidemiologic surveys.
Fecal microbiota DNA extraction, 16S rRNA gene sequencing, and shotgun metagenomic sequencing In the GNHS, fecal DNA of participants was extracted according to the protocol [ 17 ]. Measurements of targeted serum metabolome and inflammatory cytokines in the GNHS We performed targeted metabolomics to quantify the concentrations of serum metabolites among participants using an ultra-performance liquid chromatography coupled to tandem mass spectrometry system ACQUITY UPLC-Xevo TQ-S, Waters Corp.
MRI acquisition, image pre-processing and voxel-based morphometry analysis in the GNHS In the GNHS participants, 3D T1-weighted structural images were acquired with the magnetization prepared rapid acquisition gradient echo sequence on a 3.
Statistical analysis Statistical analysis was performed using Stata 15 StataCorp, College Station, TX or R software version 4. Results The overviews of the study design and multi-omics datasets are shown in Fig. Full size image. Discussion In the present study, we found significant differences in the gut microbial composition among people with different cognitive status and revealed that increased intra-individual alterations in gut microbial composition was associated with cognitive decline.
Conclusions Overall, the present study provides important evidence supporting the close association of gut microbiome with cognitive impairment and alterations of brain structure. References Patterson C. Google Scholar Bateman RJ, Xiong C, Benzinger TL, Fagan AM, Goate A, Fox NC, et al.
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