General Information:
Id: | 7,598 |
Diseases: |
Alzheimer disease
- [OMIM]
Gastrointestinal Mental Metabolic |
Mammalia | |
review | |
Reference: | Pistollato F et al.(2016) Role of gut microbiota and nutrients in amyloid formation and pathogenesis of Alzheimer disease Nutr. Rev. 74: 624-634 [PMID: 27634977] |
Interaction Information:
Comment | The gut microbiota plays a fundamental role in the modulation of the bidirectional signaling underlying the gut-brain axis. Dysbiosis and alterations of the gut microbiome composition have been shown to contribute to the development of several diseases in humans, such as inflammatory bowel disease, type 2 diabetes, metabolic syndrome, obesity, allergies, colorectal cancer, and Alzheimer disease (AD). |
Formal Description Interaction-ID: 75841 |
environment gut microbiota affects_activity of process microbiota-gut-brain axis |
Comment | Alterations of the gut microbiome can activate proinflammatory cytokines and increase intestinal permeability, leading to the development of insulin resistance, which has also been associated with AD. |
Formal Description Interaction-ID: 76438 |
environment altered gut microbiota composition increases_activity of gene/protein Proinflammatory cytokine |
Comment | The gut and the brain are deeply interconnected through the gut-brain axis. The gut-brain axis is controlled by the gut microbiota, which is composed of as many as 10(14) microorganisms, mainly bacteria belonging to about 1000 different species, but also bacteriophage particles, viruses, fungi, and archaea. The gut microbiome plays an essential role in preserving a normal gut physiology and in modulating signaling along the gut-brain axis, thus contributing to the health of the individual. |
Formal Description Interaction-ID: 76440 |
|
Comment | It has been shown that bacteria populating the gut microbiota can release significant amounts of amyloids and lipopolysaccharides, which might play a role in the modulation of signaling pathways and the production of proinflammatory cytokines related to the pathogenesis of Alzheimer disease. Additionally, nutrients have been shown to affect the composition of the gut microbiota as well as the formation and aggregation of cerebral amyloid-beta. |
Formal Description Interaction-ID: 76441 |
environment nutrients affects_quantity of environment gut microbiota |
Comment | Microbial amyloids are implicated in molecular and cellular adaptation, stimulation of adhesion, aggregation, formation of biofilm, tissue invasion, bacterial colonization, and infectivity of pathogens. Escherichia coli, Salmonella enterica, Salmonella typhimurium, Bacillus subtilis, Mycobacterium tuberculosis, and Staphylococcus aureus are some of the many bacterial strains that produce functional extracellular amyloid fibers. These bacteria might interact with the host environment in multiple ways. In particular, the E. coli endotoxin was found to potentiate the formation of Abeta fibrils in vitro and, for this reason, might be implicated in the pathogenesis of AD. |
Formal Description Interaction-ID: 76442 |
environment Escherichia coli increases_quantity of gene/protein Amyloid proteins, microbial |
Comment | Amyloid brain influx through the blood‚Äďbrain barrier is known to be mediated by the receptor for advanced glycosylation products (RAGE) and is dependent on amyloid chaperones and apolipoproteins E and J, while amyloid clearance is controlled by the low-density lipoprotein receptor-related protein 1. These transportation mechanisms are known to be altered in AD patients. |
Formal Description Interaction-ID: 76443 |
gene/protein increases_transport of gene/protein Amyloid proteins |
Comment | During aging, the composition of the gut microbiota changes, with numbers of Bacteroidetes increasing over those of Firmicutes and Bifidobacteria, even though high interindividual variations among the elderly can be found. This variability can be influenced by different dietetic regimens and different residential situations (ie, day-hospital, community, rehabilitation, or long-term residential care). |
Formal Description Interaction-ID: 76455 |
process affects_quantity of environment gut microbiota |
Comment | Some bacterial species, such as Lactobacillus and Bifidobacterium (both gram-positive facultative anaerobic or microaerophilic bacteria), can metabolize glutamate to produce gamma aminobutyric acid (GABA), the major inhibitory neurotransmitter, and alterations of gut microbiota might compromise the endogenous production of GABA and short-chain fatty acids (ie, acetate, butyrate, and propionate). |
Formal Description Interaction-ID: 76458 |
|
Comment | Alterations of GABA signaling are linked to cognitive impairment, AD, anxiety, depression, and synaptogenesis impairments, while lower levels of short-chain fatty acids might negatively affect brain glucose and energy homeostasis, immune responses, and epithelial cell growth, possibly impacting the functioning of both the central and peripheral nervous systems. |
Formal Description Interaction-ID: 76460 |
phenotype altered gamma-aminobutyric acid signaling pathway cooccurs with phenotype cognitive impairment |
Comment | Remarkably, brain-derived neurotrophic factor (BDNF) signaling was decreased in both the brain and the serum of patients affected by AD, and BDNF expression was reduced in the hippocampus of a germ-free mouse model (ie, mice that have not been naturally colonized by microorganisms). |
Formal Description Interaction-ID: 76461 |
disease decreases_activity of |
Comment | Gut cyanobacteria are known to produce the nonproteinogenic amino acid beta-N-methylamino-L-alanine, a neurotoxin known to elicit excitotoxicity by interacting with the N-methyl-D-aspartate glutamate receptor, and N-methyl-D-aspartate signaling is known to be disrupted in AD and other neuropathologies. Accordingly, high levels of beta-N-methylamino-L-alanine have been found in the brains of persons affected by AD and amyotrophic lateral sclerosis. |
Formal Description Interaction-ID: 76462 |
environment gut cyanobacteria increases_quantity of drug/chemical compound BMAA |
Comment | Gut microorganisms might also translocate from the gastrointestinal tract through microfold cells overlaying the Peyer’s patches and into the blood and other tissues, a phenomenon known as atopobiosis. This may contribute to the dynamics of inflammatory diseases such as irritable bowel syndrome, necrotizing enterocolitis, and neuroinflammatory diseases. Analogously, coccus-shaped bacteria have been found in blood samples of AD patients, particularly on the cell surface of both leukocytes and erythrocytes as well as within erythrocytes, as shown by transmission electron microscopy. |
Formal Description Interaction-ID: 76463 |
disease cooccurs with phenotype increased coccus-shaped bacteria level |
Comment | The gut microbiota plays a fundamental role in the modulation of the bidirectional signaling underlying the gut‚Äďbrain axis. Dysbiosis and alterations of the gut microbiome composition have been shown to contribute to the development of several diseases in humans, such as inflammatory bowel disease, type 2 diabetes, metabolic syndrome, obesity, allergies, colorectal cancer, and Alzheimer disease (AD). |
Formal Description Interaction-ID: 76464 |
environment altered gut microbiota composition affects_activity of environment gut dysbiosis |
Comment | The gut microbiota plays a fundamental role in the modulation of the bidirectional signaling underlying the gut‚Äďbrain axis. Dysbiosis and alterations of the gut microbiome composition have been shown to contribute to the development of several diseases in humans, such as inflammatory bowel disease, type 2 diabetes, metabolic syndrome, obesity, allergies, colorectal cancer, and Alzheimer disease (AD). |
Formal Description Interaction-ID: 76467 |
environment gut dysbiosis increases_activity of disease Inflammatory bowel disease |
Comment | The gut microbiota plays a fundamental role in the modulation of the bidirectional signaling underlying the gut‚Äďbrain axis. Dysbiosis and alterations of the gut microbiome composition have been shown to contribute to the development of several diseases in humans, such as inflammatory bowel disease, type 2 diabetes, metabolic syndrome, obesity, allergies, colorectal cancer, and Alzheimer disease (AD). |
Formal Description Interaction-ID: 76468 |
|
Comment | The gut microbiota plays a fundamental role in the modulation of the bidirectional signaling underlying the gut‚Äďbrain axis. Dysbiosis and alterations of the gut microbiome composition have been shown to contribute to the development of several diseases in humans, such as inflammatory bowel disease, type 2 diabetes, metabolic syndrome, obesity, allergies, colorectal cancer, and Alzheimer disease (AD). |
Formal Description Interaction-ID: 76469 |
environment gut dysbiosis increases_activity of disease Metabolic syndrome |
Comment | The gut microbiota plays a fundamental role in the modulation of the bidirectional signaling underlying the gut‚Äďbrain axis. Dysbiosis and alterations of the gut microbiome composition have been shown to contribute to the development of several diseases in humans, such as inflammatory bowel disease, type 2 diabetes, metabolic syndrome, obesity, allergies, colorectal cancer, and Alzheimer disease (AD). |
Formal Description Interaction-ID: 76470 |
|
Comment | The gut microbiota plays a fundamental role in the modulation of the bidirectional signaling underlying the gut‚Äďbrain axis. Dysbiosis and alterations of the gut microbiome composition have been shown to contribute to the development of several diseases in humans, such as inflammatory bowel disease, type 2 diabetes, metabolic syndrome, obesity, allergies, colorectal cancer, and Alzheimer disease (AD). |
Formal Description Interaction-ID: 76471 |
environment gut dysbiosis increases_activity of phenotype allergic reaction |
Comment | The gut microbiota plays a fundamental role in the modulation of the bidirectional signaling underlying the gut‚Äďbrain axis. Dysbiosis and alterations of the gut microbiome composition have been shown to contribute to the development of several diseases in humans, such as inflammatory bowel disease, type 2 diabetes, metabolic syndrome, obesity, allergies, colorectal cancer, and Alzheimer disease (AD). |
Formal Description Interaction-ID: 76472 |
|
Comment | The gut microbiota plays a fundamental role in the modulation of the bidirectional signaling underlying the gut‚Äďbrain axis. Dysbiosis and alterations of the gut microbiome composition have been shown to contribute to the development of several diseases in humans, such as inflammatory bowel disease, type 2 diabetes, metabolic syndrome, obesity, allergies, colorectal cancer, and Alzheimer disease (AD). |
Formal Description Interaction-ID: 76473 |
|
Comment | Alterations of the gut microbiome can activate proinflammatory cytokines and increase intestinal permeability, leading to the development of insulin resistance, which has also been associated with AD. |
Formal Description Interaction-ID: 76479 |
environment altered gut microbiota composition increases_activity of phenotype increased intestinal permeability |
Comment | Alterations of the gut microbiome can activate proinflammatory cytokines and increase intestinal permeability, leading to the development of insulin resistance, which has also been associated with AD. |
Formal Description Interaction-ID: 76480 |
|
Comment | The gut and the brain are deeply interconnected through the gut-brain axis. The gut-brain axis is controlled by the gut microbiota, which is composed of as many as 10(14) microorganisms, mainly bacteria belonging to about 1000 different species, but also bacteriophage particles, viruses, fungi, and archaea. The gut microbiome plays an essential role in preserving a normal gut physiology and in modulating signaling along the gut-brain axis, thus contributing to the health of the individual. |
Formal Description Interaction-ID: 76488 |
|
Comment | It has been shown that bacteria populating the gut microbiota can release significant amounts of amyloids and lipopolysaccharides, which might play a role in the modulation of signaling pathways and the production of proinflammatory cytokines related to the pathogenesis of Alzheimer disease. Additionally, nutrients have been shown to affect the composition of the gut microbiota as well as the formation and aggregation of cerebral amyloid-beta. |
Formal Description Interaction-ID: 76524 |
|
Comment | Nutrients have been shown to affect the composition of the gut microbiota as well as the formation and aggregation of cerebral amyloid-beta. |
Formal Description Interaction-ID: 76525 |
|
Comment | Escherichia coli, Salmonella enterica, Salmonella typhimurium, Bacillus subtilis, Mycobacterium tuberculosis, and Staphylococcus aureus are some of the many bacterial strains that produce functional extracellular amyloid fibers. These bacteria might interact with the host environment in multiple ways. |
Formal Description Interaction-ID: 76526 |
environment Salmonella enterica increases_quantity of phenotype |
Comment | Escherichia coli, Salmonella enterica, Salmonella typhimurium, Bacillus subtilis, Mycobacterium tuberculosis, and Staphylococcus aureus are some of the many bacterial strains that produce functional extracellular amyloid fibers. These bacteria might interact with the host environment in multiple ways. |
Formal Description Interaction-ID: 76527 |
environment Salmonella typhimurium increases_quantity of phenotype |
Comment | Escherichia coli, Salmonella enterica, Salmonella typhimurium, Bacillus subtilis, Mycobacterium tuberculosis, and Staphylococcus aureus are some of the many bacterial strains that produce functional extracellular amyloid fibers. These bacteria might interact with the host environment in multiple ways. |
Formal Description Interaction-ID: 76528 |
environment Bacillus subtilis increases_quantity of phenotype |
Comment | Escherichia coli, Salmonella enterica, Salmonella typhimurium, Bacillus subtilis, Mycobacterium tuberculosis, and Staphylococcus aureus are some of the many bacterial strains that produce functional extracellular amyloid fibers. These bacteria might interact with the host environment in multiple ways. |
Formal Description Interaction-ID: 76529 |
environment Mycobacterium tuberculosis increases_quantity of phenotype |
Comment | Escherichia coli, Salmonella enterica, Salmonella typhimurium, Bacillus subtilis, Mycobacterium tuberculosis, and Staphylococcus aureus are some of the many bacterial strains that produce functional extracellular amyloid fibers. These bacteria might interact with the host environment in multiple ways. |
Formal Description Interaction-ID: 76530 |
environment Staphylococcus aureus increases_quantity of phenotype |
Comment | Amyloid brain influx through the blood‚Äďbrain barrier is known to be mediated by the receptor for advanced glycosylation products (RAGE) and is dependent on amyloid chaperones and apolipoproteins E and J, while amyloid clearance is controlled by the low-density lipoprotein receptor-related protein 1. These transportation mechanisms are known to be altered in AD patients. |
Formal Description Interaction-ID: 77097 |
gene/protein increases_activity of process Amyloid protein import |
Comment | Amyloid brain influx through the blood‚Äďbrain barrier is known to be mediated by the receptor for advanced glycosylation products (RAGE) and is dependent on amyloid chaperones and apolipoproteins E and J, while amyloid clearance is controlled by the low-density lipoprotein receptor-related protein 1. These transportation mechanisms are known to be altered in AD patients. |
Formal Description Interaction-ID: 77098 |
gene/protein amyloid chaperone increases_activity of process Amyloid protein import |
Comment | Amyloid brain influx through the blood‚Äďbrain barrier is known to be mediated by the receptor for advanced glycosylation products (RAGE) and is dependent on amyloid chaperones and apolipoproteins E and J, while amyloid clearance is controlled by the low-density lipoprotein receptor-related protein 1. These transportation mechanisms are known to be altered in AD patients. |
Formal Description Interaction-ID: 77099 |
|
Drugbank entries | Show/Hide entries for APOE |
Comment | Amyloid brain influx through the blood‚Äďbrain barrier is known to be mediated by the receptor for advanced glycosylation products (RAGE) and is dependent on amyloid chaperones and apolipoproteins E and J, while amyloid clearance is controlled by the low-density lipoprotein receptor-related protein 1. These transportation mechanisms are known to be altered in AD patients. |
Formal Description Interaction-ID: 77100 |
|
Comment | Amyloid brain influx through the blood‚Äďbrain barrier is known to be mediated by the receptor for advanced glycosylation products (RAGE) and is dependent on amyloid chaperones and apolipoproteins E and J, while amyloid clearance is controlled by the low-density lipoprotein receptor-related protein 1. These transportation mechanisms are known to be altered in AD patients. |
Formal Description Interaction-ID: 77101 |
|
Drugbank entries | Show/Hide entries for LRP1 |
Comment | During aging, the composition of the gut microbiota changes, with numbers of Bacteroidetes increasing over those of Firmicutes and Bifidobacteria, even though high interindividual variations among the elderly can be found. This variability can be influenced by different dietetic regimens and different residential situations (ie, day-hospital, community, rehabilitation, or long-term residential care). |
Formal Description Interaction-ID: 77102 |
process increases_quantity of environment Bacteroidetes |
Comment | During aging, the composition of the gut microbiota changes, with numbers of Bacteroidetes increasing over those of Firmicutes and Bifidobacteria, even though high interindividual variations among the elderly can be found. This variability can be influenced by different dietetic regimens and different residential situations (ie, day-hospital, community, rehabilitation, or long-term residential care). |
Formal Description Interaction-ID: 77103 |
|
Comment | During aging, the composition of the gut microbiota changes, with numbers of Bacteroidetes increasing over those of Firmicutes and Bifidobacteria, even though high interindividual variations among the elderly can be found. This variability can be influenced by different dietetic regimens and different residential situations (ie, day-hospital, community, rehabilitation, or long-term residential care). |
Formal Description Interaction-ID: 77104 |
process decreases_quantity of environment Bifidobacterium |
Comment | Alterations of GABA signaling are linked to cognitive impairment, AD, anxiety, depression, and synaptogenesis impairments, while lower levels of short-chain fatty acids might negatively affect brain glucose and energy homeostasis, immune responses, and epithelial cell growth, possibly impacting the functioning of both the central and peripheral nervous systems. |
Formal Description Interaction-ID: 77197 |
disease increases_activity of phenotype altered gamma-aminobutyric acid signaling pathway |
Comment | Alterations of GABA signaling are linked to cognitive impairment, AD, anxiety, depression, and synaptogenesis impairments, while lower levels of short-chain fatty acids might negatively affect brain glucose and energy homeostasis, immune responses, and epithelial cell growth, possibly impacting the functioning of both the central and peripheral nervous systems. |
Formal Description Interaction-ID: 77198 |
phenotype increases_activity of phenotype altered gamma-aminobutyric acid signaling pathway |
Comment | Alterations of GABA signaling are linked to cognitive impairment, AD, anxiety, depression, and synaptogenesis impairments, while lower levels of short-chain fatty acids might negatively affect brain glucose and energy homeostasis, immune responses, and epithelial cell growth, possibly impacting the functioning of both the central and peripheral nervous systems. |
Formal Description Interaction-ID: 77199 |
phenotype increases_activity of phenotype altered gamma-aminobutyric acid signaling pathway |
Comment | Alterations of GABA signaling are linked to cognitive impairment, AD, anxiety, depression, and synaptogenesis impairments, while lower levels of short-chain fatty acids might negatively affect brain glucose and energy homeostasis, immune responses, and epithelial cell growth, possibly impacting the functioning of both the central and peripheral nervous systems. |
Formal Description Interaction-ID: 77200 |
phenotype synapse assembly impairment increases_activity of phenotype altered gamma-aminobutyric acid signaling pathway |
Comment | Remarkably, brain-derived neurotrophic factor (BDNF) signaling was decreased in both the brain and the serum of patients affected by AD, and BDNF expression was reduced in the hippocampus of a germ-free mouse model (ie, mice that have not been naturally colonized by microorganisms). |
Formal Description Interaction-ID: 77201 |
disease decreases_expression of gene/protein |
Comment | Gut cyanobacteria are known to produce the nonproteinogenic amino acid beta-N-methylamino-Lalanine, a neurotoxin known to elicit excitotoxicity by interacting with the N-methyl-D-aspartate glutamate receptor, and N-methyl-D-aspartate signaling is known to be disrupted in AD and other neuropathologies. Accordingly, high levels of beta-N-methylamino-L-alanine have been found in the brains of persons affected by AD and amyotrophic lateral sclerosis. |
Formal Description Interaction-ID: 77202 |
drug/chemical compound BMAA increases_activity of |
Comment | Gut cyanobacteria are known to produce the nonproteinogenic amino acid beta-N-methylamino-L-alanine, a neurotoxin known to elicit excitotoxicity by interacting with the N-methyl-D-aspartate glutamate receptor, and N-methyl-D-aspartate signaling is known to be disrupted in AD and other neuropathologies. Accordingly, high levels of beta-N-methylamino-L-alanine have been found in the brains of persons affected by AD and amyotrophic lateral sclerosis. |
Formal Description Interaction-ID: 77203 |
drug/chemical compound BMAA interacts (colocalizes) with complex/PPI NMDA receptor complex |
Comment | Gut cyanobacteria are known to produce the nonproteinogenic amino acid beta-N-methylamino-L-alanine, a neurotoxin known to elicit excitotoxicity by interacting with the N-methyl-D-aspartate glutamate receptor, and N-methyl-D-aspartate signaling is known to be disrupted in AD and other neuropathologies. Accordingly, high levels of beta-N-methylamino-L-alanine have been found in the brains of persons affected by AD and amyotrophic lateral sclerosis. |
Formal Description Interaction-ID: 77204 |
|
Comment | Gut cyanobacteria are known to produce the nonproteinogenic amino acid beta-N-methylamino-L-alanine, a neurotoxin known to elicit excitotoxicity by interacting with the N-methyl-D-aspartate glutamate receptor, and N-methyl-D-aspartate signaling is known to be disrupted in AD and other neuropathologies. Accordingly, high levels of beta-N-methylamino-L-alanine have been found in the brains of persons affected by AD and amyotrophic lateral sclerosis. |
Formal Description Interaction-ID: 77205 |
disease increases_quantity of drug/chemical compound BMAA |
Comment | Gut cyanobacteria are known to produce the nonproteinogenic amino acid beta-N-methylamino-L-alanine, a neurotoxin known to elicit excitotoxicity by interacting with the N-methyl-D-aspartate glutamate receptor, and N-methyl-D-aspartate signaling is known to be disrupted in AD and other neuropathologies. Accordingly, high levels of beta-N-methylamino-L-alanine have been found in the brains of persons affected by AD and amyotrophic lateral sclerosis. |
Formal Description Interaction-ID: 77210 |
disease Amyotrophic lateral sclerosis increases_quantity of drug/chemical compound BMAA |
Comment | While foods such as fructose- and purine-rich foods can stimulate the generation of uric acid, thus causing insulin resistance and fat accumulation, others (eg, plant foods, antioxidants, probiotics, nuts, soybeans, and n-3 fatty acids) can positively modulate mitochondrial biogenesis. |
Formal Description Interaction-ID: 77262 |
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Comment | n-3 polyunsaturated fatty acids are known to have important anti-inflammatory and immunomodulatory properties and have been used for the prevention and treatment of diseases characterized by chronic gut inflammation (eg, irritable bowel syndrome and rheumatoid arthritis) and neurodegeneration (eg. AD). |
Formal Description Interaction-ID: 77263 |
drug/chemical compound Polyunsaturated fatty acid, omega-3 decreases_activity of process |
Comment | Diet can affect the composition of the gut microbiota. |
Formal Description Interaction-ID: 77264 |
environment diet affects_quantity of environment gut microbiota |
Comment | Diets characterized by high intakes of fruit and vegetables (eg, rural, Mediterranean, plant-rich, or plant-based diets) and a low or null consumption of meat are associated with a greater abundance of Prevotella than Bacteroides organisms. |
Formal Description Interaction-ID: 77266 |
environment plant-rich diet increases_quantity of environment Prevotella bacteria |
Comment | Bacteroides bacteria are enriched with genes necessary for breaking down amino acids. For this reason, Bacteroides species seem more prevalent in Western populations that follow a Western-style diet, rich in animal proteins and fats and low in fiber, confirming the key role of diet as a modulator of the gut microbiota composition. |
Formal Description Interaction-ID: 77267 |
environment Bacteroides increases_expression of gene/protein genes involved in breaking down amino acids |
Comment | Probiotics and prebiotics can stimulate the growth of Bifidobacterium populations while concomitantly decreasing the growth of enterobacteria. |
Formal Description Interaction-ID: 77271 |
environment prebiotic diet increases_quantity of environment Bifidobacterium |
Comment | Probiotics were also found to decrease levels of proinflammatory cytokines such as IL-5, IL-6, IL-1b, IL-8, and TNF-aLpha, which are upregulated in the elderly, and to increase levels of natural killer cells, activated lymphocytes, and phagocytosis, suggesting improvement of the adaptive immune response and reduction of inflammation. |
Formal Description Interaction-ID: 77272 |
|
Drugbank entries | Show/Hide entries for IL5 |
Comment | Supplementation with probiotics was reported to reduce the levels of von Willebrand factor (a blood glycoprotein found elevated in cardiovascular, cancer, and connective tissue-related diseases) and to significantly upregulate the protein BDNF and the cytokines MCP-1 (monocyte chemotactic protein-1) and CCL5/RANTES (chemokine [C-C motif] ligand5 / regulated on activation, normal T cell expressed and secreted), both related to IL-17, as well as the chemokine MIP-1b (macrophage inflammatory protein-1b), in schizophrenia patients, reducing gastrointestinal leakage. |
Formal Description Interaction-ID: 77274 |
environment Probiotics decreases_quantity of gene/protein |
Drugbank entries | Show/Hide entries for VWF |
Comment | BDNF was downregulated in the brains of AD patients. |
Formal Description Interaction-ID: 77276 |
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Comment | A clinical intervention trial involving 6 obese subjects with type 2 diabetes and/or hypertension who followed a strict vegetarian diet for 1 month showed that the vegetarian diet promoted a reduction of gut inflammation, with a decrease of pathobionts (ie, Enterobacteriaceae) and an increase of commensal microbes (ie, Bacteroides fragilis and Clostridium species belonging to clusters XIVa and IV). This resulted in a reduction of intestinal lipocalin-2, an adipokine associated with the development of inflammation and insulin resistance, and higher levels of short-chain fatty acids, which are associated with improved glucose homeostasis and insulin sensitivity as well as modulation of CNS functions, as reported above. |
Formal Description Interaction-ID: 77278 |
environment vegetarian diet decreases_activity of phenotype gut inflammation |
Comment | Clinically and cognitively normal individuals with and without AD risk factors, following dietary patterns characterized by high intakes of whole grains, fresh fruits, vegetables, legumes, fish, and low-fat dairy products (which provide higher intakes of vitamin B12, vitamin D, and n-3 polyunsaturated fatty acids) and by low intakes of refined sugars, French fries, highfat dairy products, butter, and processed meat, show lower accumulation of Abeta in the brain and higher cerebral glucose metabolism, as evidenced by neuroimaging analysis of gray matter volumes (a marker of brain atrophy), 11C-Pittsburgh compound B (to measure the accumulation of fibrillar Abeta), and 8F-fluorodeoxyglucose (to assess brain glucose metabolism). |
Formal Description Interaction-ID: 77279 |
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Comment | Several studies have described the beneficial effects of natural phenols present in plant-derived foods, such as green tea, red berries, spices, extra virgin olive oil, red wine, and aromatic herbs, in reducing amyloid aggregation and the incidence of amyloid-related diseases. |
Formal Description Interaction-ID: 77281 |
drug/chemical compound Natural phenols decreases_quantity of phenotype amyloid aggregation |
Comment | In particular, oleuropein aglycone and oleocanthal, two phenolic components of extra virgin olive oil, have been shown to promote Abeta clearance and autophagy as well as inhibition of tau aggregation and neuroinflammation. |
Formal Description Interaction-ID: 77282 |
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Comment | Oleocanthal has been found to stimulate Abeta clearance by upregulating two major transporters of Abeta expressed in the blood‚Äďbrain barrier (ie,P-glycoprotein and low-density lipoprotein receptor-related protein 1), consequently increasing the brain efflux rate, as shown in murine brain endothelial cells in vitro and in C57BL/6 wild-type mice in vivo. |
Formal Description Interaction-ID: 77283 |
drug/chemical compound Oleocanthal increases_expression of gene/protein |
Drugbank entries | Show/Hide entries for ABCB1 |
Comment | Gallic acid, the most active component in grape seed extracts, has been shown to inhibit fibrillary aggregation of both Abeta peptides and kappa-casein (a milk protein known to spontaneously form amyloid fibrils under physiological conditions) in vitro. |
Formal Description Interaction-ID: 77287 |
drug/chemical compound decreases_activity of process |
Comment | Tea phenolics and their aromatic metabolites have been reported to elicit bacteriostatic or antimicrobial activities on gut microbiota, specifically inhibiting the growth of some pathogenic bacteria (ie, Clostridium perfringens, Clostridium difficile, and Bacteroides species). |
Formal Description Interaction-ID: 77290 |
drug/chemical compound Tea phenolics decreases_quantity of environment Clostridium perfringens |
Comment | While foods such as fructose- and purine-rich foods can stimulate the generation of uric acid, thus causing insulin resistance and fat accumulation, others (eg, plant foods, antioxidants, probiotics, nuts, soybeans, and n-3 fatty acids) can positively modulate mitochondrial biogenesis. |
Formal Description Interaction-ID: 77380 |
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Comment | While foods such as fructose- and purine-rich foods can stimulate the generation of uric acid, thus causing insulin resistance and fat accumulation, others (eg, plant foods, antioxidants, probiotics, nuts, soybeans, and n-3 fatty acids) can positively modulate mitochondrial biogenesis. |
Formal Description Interaction-ID: 77381 |
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Comment | While foods such as fructose- and purine-rich foods can stimulate the generation of uric acid, thus causing insulin resistance and fat accumulation, others (eg, plant foods, antioxidants, probiotics, nuts, soybeans, and n-3 fatty acids) can positively modulate mitochondrial biogenesis. |
Formal Description Interaction-ID: 77382 |
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Comment | While foods such as fructose- and purine-rich foods can stimulate the generation of uric acid, thus causing insulin resistance and fat accumulation, others (eg, plant foods, antioxidants, probiotics, nuts, soybeans, and n-3 fatty acids) can positively modulate mitochondrial biogenesis. |
Formal Description Interaction-ID: 77383 |
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Comment | While foods such as fructose- and purine-rich foods can stimulate the generation of uric acid, thus causing insulin resistance and fat accumulation, others (eg, plant foods, antioxidants, probiotics, nuts, soybeans, and n-3 fatty acids) can positively modulate mitochondrial biogenesis. |
Formal Description Interaction-ID: 77384 |
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Comment | While foods such as fructose- and purine-rich foods can stimulate the generation of uric acid, thus causing insulin resistance and fat accumulation, others (eg, plant foods, antioxidants, probiotics, nuts, soybeans, and n-3 fatty acids) can positively modulate mitochondrial biogenesis. |
Formal Description Interaction-ID: 77390 |
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Comment | While foods such as fructose- and purine-rich foods can stimulate the generation of uric acid, thus causing insulin resistance and fat accumulation, others (eg, plant foods, antioxidants, probiotics, nuts, soybeans, and n-3 fatty acids) can positively modulate mitochondrial biogenesis. |
Formal Description Interaction-ID: 77392 |
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Comment | While foods such as fructose- and purine-rich foods can stimulate the generation of uric acid, thus causing insulin resistance and fat accumulation, others (eg, plant foods, antioxidants, probiotics, nuts, soybeans, and n-3 fatty acids) can positively modulate mitochondrial biogenesis. |
Formal Description Interaction-ID: 77395 |
environment plant-rich diet increases_activity of process mitochondrial biogenesis |
Comment | While foods such as fructose- and purine-rich foods can stimulate the generation of uric acid, thus causing insulin resistance and fat accumulation, others (eg, plant foods, antioxidants, probiotics, nuts, soybeans, and n-3 fatty acids) can positively modulate mitochondrial biogenesis. |
Formal Description Interaction-ID: 77397 |
environment antioxidant diet increases_activity of process mitochondrial biogenesis |
Comment | While foods such as fructose- and purine-rich foods can stimulate the generation of uric acid, thus causing insulin resistance and fat accumulation, others (eg, plant foods, antioxidants, probiotics, nuts, soybeans, and n-3 fatty acids) can positively modulate mitochondrial biogenesis. |
Formal Description Interaction-ID: 77400 |
environment Probiotics increases_activity of process mitochondrial biogenesis |
Comment | While foods such as fructose- and purine-rich foods can stimulate the generation of uric acid, thus causing insulin resistance and fat accumulation, others (eg, plant foods, antioxidants, probiotics, nuts, soybeans, and n-3 fatty acids) can positively modulate mitochondrial biogenesis. |
Formal Description Interaction-ID: 77402 |
environment nut-rich diet increases_activity of process mitochondrial biogenesis |
Comment | While foods such as fructose- and purine-rich foods can stimulate the generation of uric acid, thus causing insulin resistance and fat accumulation, others (eg, plant foods, antioxidants, probiotics, nuts, soybeans, and n-3 fatty acids) can positively modulate mitochondrial biogenesis. |
Formal Description Interaction-ID: 77403 |
environment soybean-rich diet increases_activity of process mitochondrial biogenesis |
Comment | While foods such as fructose- and purine-rich foods can stimulate the generation of uric acid, thus causing insulin resistance and fat accumulation, others (eg, plant foods, antioxidants, probiotics, nuts, soybeans, and n-3 fatty acids) can positively modulate mitochondrial biogenesis. |
Formal Description Interaction-ID: 77404 |
environment n-3 fatty acid-rich diet increases_activity of process mitochondrial biogenesis |
Comment | n-3 polyunsaturated fatty acids are known to have important anti-inflammatory and immunomodulatory properties and have been used for the prevention and treatment of diseases characterized by chronic gut inflammation (eg, irritable bowel syndrome and rheumatoid arthritis) and neurodegeneration (eg. AD). |
Formal Description Interaction-ID: 77410 |
drug/chemical compound Polyunsaturated fatty acid, omega-3 increases_activity of phenotype immunomodulatory properties |
Comment | n-3 polyunsaturated fatty acids are known to have important anti-inflammatory and immunomodulatory properties and have been used for the prevention and treatment of diseases characterized by chronic gut inflammation (eg, irritable bowel syndrome and rheumatoid arthritis) and neurodegeneration (eg. AD). |
Formal Description Interaction-ID: 77412 |
drug/chemical compound Polyunsaturated fatty acid, omega-3 decreases_activity of disease |
Comment | n-3 polyunsaturated fatty acids are known to have important anti-inflammatory and immunomodulatory properties and have been used for the prevention and treatment of diseases characterized by chronic gut inflammation (eg, irritable bowel syndrome and rheumatoid arthritis) and neurodegeneration (eg. AD). |
Formal Description Interaction-ID: 77413 |
drug/chemical compound Polyunsaturated fatty acid, omega-3 decreases_activity of disease Irritable bowel syndrome |
Comment | n-3 polyunsaturated fatty acids are known to have important anti-inflammatory and immunomodulatory properties and have been used for the prevention and treatment of diseases characterized by chronic gut inflammation (eg, irritable bowel syndrome and rheumatoid arthritis) and neurodegeneration (eg. AD). |
Formal Description Interaction-ID: 77415 |
drug/chemical compound Polyunsaturated fatty acid, omega-3 decreases_activity of disease |
Comment | Bacteria from the genus Prevotella are known to express genes controlling cellulose and xylan hydrolysis. |
Formal Description Interaction-ID: 77545 |
environment Prevotella bacteria increases_expression of gene/protein genes involved in cellulose and xylan hydrolysis |
Comment | Bacteroides bacteria are enriched with genes necessary for breaking down amino acids. For this reason, Bacteroides species seem more prevalent in Western populations that follow a Western-style diet, rich in animal proteins and fats and low in fiber, confirming the key role of diet as a modulator of the gut microbiota composition. |
Formal Description Interaction-ID: 77546 |
environment Western-style diet increases_quantity of environment Bacteroides |
Comment | Probiotics and prebiotics can stimulate the growth of Bifidobacterium populations while concomitantly decreasing the growth of enterobacteria. |
Formal Description Interaction-ID: 77547 |
environment prebiotic diet increases_quantity of environment Bifidobacterium |
Comment | Probiotics and prebiotics can stimulate the growth of Bifidobacterium populations while concomitantly decreasing the growth of enterobacteria. |
Formal Description Interaction-ID: 77548 |
environment Probiotics decreases_quantity of environment Enterobacteria |
Comment | Probiotics and prebiotics can stimulate the growth of Bifidobacterium populations while concomitantly decreasing the growth of enterobacteria. |
Formal Description Interaction-ID: 77549 |
environment prebiotic diet decreases_quantity of environment Enterobacteria |
Comment | Probiotics were also found to decrease levels of proinflammatory cytokines such as IL-5, IL-6, IL-1b, IL-8, and TNF-aLpha, which are upregulated in the elderly, and to increase levels of natural killer cells, activated lymphocytes, and phagocytosis, suggesting improvement of the adaptive immune response and reduction of inflammation. |
Formal Description Interaction-ID: 77550 |
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Drugbank entries | Show/Hide entries for IL6 |
Comment | Probiotics were also found to decrease levels of proinflammatory cytokines such as IL-5, IL-6, IL-1b, IL-8, and TNF-aLpha, which are upregulated in the elderly, and to increase levels of natural killer cells, activated lymphocytes, and phagocytosis, suggesting improvement of the adaptive immune response and reduction of inflammation. |
Formal Description Interaction-ID: 77551 |
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Drugbank entries | Show/Hide entries for IL1B |
Comment | Probiotics were also found to decrease levels of proinflammatory cytokines such as IL-5, IL-6, IL-1b, IL-8, and TNF-aLpha, which are upregulated in the elderly, and to increase levels of natural killer cells, activated lymphocytes, and phagocytosis, suggesting improvement of the adaptive immune response and reduction of inflammation. |
Formal Description Interaction-ID: 77552 |
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Comment | Probiotics were also found to decrease levels of proinflammatory cytokines such as IL-5, IL-6, IL-1b, IL-8, and TNF-aLpha, which are upregulated in the elderly, and to increase levels of natural killer cells, activated lymphocytes, and phagocytosis, suggesting improvement of the adaptive immune response and reduction of inflammation. |
Formal Description Interaction-ID: 77553 |
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Drugbank entries | Show/Hide entries for TNF |
Comment | Probiotics were also found to decrease levels of proinflammatory cytokines such as IL-5, IL-6, IL-1b, IL-8, and TNF-aLpha, which are upregulated in the elderly, and to increase levels of natural killer cells, activated lymphocytes, and phagocytosis, suggesting improvement of the adaptive immune response and reduction of inflammation. |
Formal Description Interaction-ID: 77554 |
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Drugbank entries | Show/Hide entries for IL5 |
Comment | Probiotics were also found to decrease levels of proinflammatory cytokines such as IL-5, IL-6, IL-1b, IL-8, and TNF-aLpha, which are upregulated in the elderly, and to increase levels of natural killer cells, activated lymphocytes, and phagocytosis, suggesting improvement of the adaptive immune response and reduction of inflammation. |
Formal Description Interaction-ID: 77555 |
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Drugbank entries | Show/Hide entries for IL6 |
Comment | Probiotics were also found to decrease levels of proinflammatory cytokines such as IL-5, IL-6, IL-1b, IL-8, and TNF-aLpha, which are upregulated in the elderly, and to increase levels of natural killer cells, activated lymphocytes, and phagocytosis, suggesting improvement of the adaptive immune response and reduction of inflammation. |
Formal Description Interaction-ID: 77556 |
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Drugbank entries | Show/Hide entries for IL1B |
Comment | Probiotics were also found to decrease levels of proinflammatory cytokines such as IL-5, IL-6, IL-1b, IL-8, and TNF-aLpha, which are upregulated in the elderly, and to increase levels of natural killer cells, activated lymphocytes, and phagocytosis, suggesting improvement of the adaptive immune response and reduction of inflammation. |
Formal Description Interaction-ID: 77557 |
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Comment | Probiotics were also found to decrease levels of proinflammatory cytokines such as IL-5, IL-6, IL-1b, IL-8, and TNF-aLpha, which are upregulated in the elderly, and to increase levels of natural killer cells, activated lymphocytes, and phagocytosis, suggesting improvement of the adaptive immune response and reduction of inflammation. |
Formal Description Interaction-ID: 77558 |
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Drugbank entries | Show/Hide entries for TNF |
Comment | Probiotics were also found to decrease levels of proinflammatory cytokines such as IL-5, IL-6, IL-1b, IL-8, and TNF-aLpha, which are upregulated in the elderly, and to increase levels of natural killer cells, activated lymphocytes, and phagocytosis, suggesting improvement of the adaptive immune response and reduction of inflammation. |
Formal Description Interaction-ID: 77559 |
|
Comment | Probiotics were also found to decrease levels of proinflammatory cytokines such as IL-5, IL-6, IL-1b, IL-8, and TNF-aLpha, which are upregulated in the elderly, and to increase levels of natural killer cells, activated lymphocytes, and phagocytosis, suggesting improvement of the adaptive immune response and reduction of inflammation. |
Formal Description Interaction-ID: 77560 |
|
Comment | Probiotics were also found to decrease levels of proinflammatory cytokines such as IL-5, IL-6, IL-1b, IL-8, and TNF-aLpha, which are upregulated in the elderly, and to increase levels of natural killer cells, activated lymphocytes, and phagocytosis, suggesting improvement of the adaptive immune response and reduction of inflammation. |
Formal Description Interaction-ID: 77561 |
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Comment | Supplementation with probiotics was reported to reduce the levels of von Willebrand factor (a blood glycoprotein found elevated in cardiovascular, cancer, and connective tissue-related diseases) and to significantly upregulate the protein BDNF and the cytokines MCP-1 (monocyte chemotactic protein-1) and CCL5/RANTES (chemokine [C-C motif] ligand5 / regulated on activation, normal T cell expressed and secreted), both related to IL-17, as well as the chemokine MIP-1b (macrophage inflammatory protein-1b), in schizophrenia patients, reducing gastrointestinal leakage. |
Formal Description Interaction-ID: 77562 |
environment Probiotics increases_expression of gene/protein |
Comment | Supplementation with probiotics was reported to reduce the levels of von Willebrand factor (a blood glycoprotein found elevated in cardiovascular, cancer, and connective tissue-related diseases) and to significantly upregulate the protein BDNF and the cytokines MCP-1 (monocyte chemotactic protein-1) and CCL5/RANTES (chemokine [C-C motif] ligand5 / regulated on activation, normal T cell expressed and secreted), both related to IL-17, as well as the chemokine MIP-1b (macrophage inflammatory protein-1b), in schizophrenia patients, reducing gastrointestinal leakage. |
Formal Description Interaction-ID: 77563 |
environment Probiotics increases_expression of gene/protein |
Drugbank entries | Show/Hide entries for CCL2 |
Comment | Supplementation with probiotics was reported to reduce the levels of von Willebrand factor (a blood glycoprotein found elevated in cardiovascular, cancer, and connective tissue-related diseases) and to significantly upregulate the protein BDNF and the cytokines MCP-1 (monocyte chemotactic protein-1) and CCL5/RANTES (chemokine [C-C motif] ligand5 / regulated on activation, normal T cell expressed and secreted), both related to IL-17, as well as the chemokine MIP-1b (macrophage inflammatory protein-1b), in schizophrenia patients, reducing gastrointestinal leakage. |
Formal Description Interaction-ID: 77564 |
environment Probiotics increases_expression of gene/protein |
Drugbank entries | Show/Hide entries for CCL5 |
Comment | Supplementation with probiotics was reported to reduce the levels of von Willebrand factor (a blood glycoprotein found elevated in cardiovascular, cancer, and connective tissue-related diseases) and to significantly upregulate the protein BDNF and the cytokines MCP-1 (monocyte chemotactic protein-1) and CCL5/RANTES (chemokine [C-C motif] ligand5 / regulated on activation, normal T cell expressed and secreted), both related to IL-17, as well as the chemokine MIP-1b (macrophage inflammatory protein-1b), in schizophrenia patients, reducing gastrointestinal leakage. |
Formal Description Interaction-ID: 77565 |
environment Probiotics increases_expression of gene/protein |
Comment | Clinically and cognitively normal individuals with and without AD risk factors, following dietary patterns characterized by high intakes of whole grains, fresh fruits, vegetables, legumes, fish, and low-fat dairy products (which provide higher intakes of vitamin B12, vitamin D, and n-3 polyunsaturated fatty acids) and by low intakes of refined sugars, French fries, highfat dairy products, butter, and processed meat, show lower accumulation of Abeta in the brain and higher cerebral glucose metabolism, as evidenced by neuroimaging analysis of gray matter volumes (a marker of brain atrophy), 11C-Pittsburgh compound B (to measure the accumulation of fibrillar Abeta), and 8F-fluorodeoxyglucose (to assess brain glucose metabolism). |
Formal Description Interaction-ID: 77571 |
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Comment | A clinical intervention trial involving 6 obese subjects with type 2 diabetes and/or hypertension who followed a strict vegetarian diet for 1 month showed that the vegetarian diet promoted a reduction of gut inflammation, with a decrease of pathobionts (ie, Enterobacteriaceae) and an increase of commensal microbes (ie, Bacteroides fragilis and Clostridium species belonging to clusters XIVa and IV). This resulted in a reduction of intestinal lipocalin-2, an adipokine associated with the development of inflammation and insulin resistance, and higher levels of short-chain fatty acids, which are associated with improved glucose homeostasis and insulin sensitivity as well as modulation of CNS functions, as reported above. |
Formal Description Interaction-ID: 77572 |
environment vegetarian diet decreases_quantity of environment pathobionts |
Comment | A clinical intervention trial involving 6 obese subjects with type 2 diabetes and/or hypertension who followed a strict vegetarian diet for 1 month showed that the vegetarian diet promoted a reduction of gut inflammation, with a decrease of pathobionts (ie, Enterobacteriaceae) and an increase of commensal microbes (ie, Bacteroides fragilis and Clostridium species belonging to clusters XIVa and IV). This resulted in a reduction of intestinal lipocalin-2, an adipokine associated with the development of inflammation and insulin resistance, and higher levels of short-chain fatty acids, which are associated with improved glucose homeostasis and insulin sensitivity as well as modulation of CNS functions, as reported above. |
Formal Description Interaction-ID: 77573 |
environment vegetarian diet decreases_quantity of environment Enterobacteriaceae |
Comment | A clinical intervention trial involving 6 obese subjects with type 2 diabetes and/or hypertension who followed a strict vegetarian diet for 1 month showed that the vegetarian diet promoted a reduction of gut inflammation, with a decrease of pathobionts (ie, Enterobacteriaceae) and an increase of commensal microbes (ie, Bacteroides fragilis and Clostridium species belonging to clusters XIVa and IV). This resulted in a reduction of intestinal lipocalin-2, an adipokine associated with the development of inflammation and insulin resistance, and higher levels of short-chain fatty acids, which are associated with improved glucose homeostasis and insulin sensitivity as well as modulation of CNS functions, as reported above. |
Formal Description Interaction-ID: 77574 |
environment vegetarian diet increases_quantity of environment Bacteroides fragilis |
Comment | A clinical intervention trial involving 6 obese subjects with type 2 diabetes and/or hypertension who followed a strict vegetarian diet for 1 month showed that the vegetarian diet promoted a reduction of gut inflammation, with a decrease of pathobionts (ie, Enterobacteriaceae) and an increase of commensal microbes (ie, Bacteroides fragilis and Clostridium species belonging to clusters XIVa and IV). This resulted in a reduction of intestinal lipocalin-2, an adipokine associated with the development of inflammation and insulin resistance, and higher levels of short-chain fatty acids, which are associated with improved glucose homeostasis and insulin sensitivity as well as modulation of CNS functions, as reported above. |
Formal Description Interaction-ID: 77575 |
environment vegetarian diet increases_quantity of environment Clostridium XIVa |
Comment | A clinical intervention trial involving 6 obese subjects with type 2 diabetes and/or hypertension who followed a strict vegetarian diet for 1 month showed that the vegetarian diet promoted a reduction of gut inflammation, with a decrease of pathobionts (ie, Enterobacteriaceae) and an increase of commensal microbes (ie, Bacteroides fragilis and Clostridium species belonging to clusters XIVa and IV). This resulted in a reduction of intestinal lipocalin-2, an adipokine associated with the development of inflammation and insulin resistance, and higher levels of short-chain fatty acids, which are associated with improved glucose homeostasis and insulin sensitivity as well as modulation of CNS functions, as reported above. |
Formal Description Interaction-ID: 77576 |
environment vegetarian diet decreases_quantity of gene/protein |
Drugbank entries | Show/Hide entries for LCN2 |
Comment | A clinical intervention trial involving 6 obese subjects with type 2 diabetes and/or hypertension who followed a strict vegetarian diet for 1 month showed that the vegetarian diet promoted a reduction of gut inflammation, with a decrease of pathobionts (ie, Enterobacteriaceae) and an increase of commensal microbes (ie, Bacteroides fragilis and Clostridium species belonging to clusters XIVa and IV). This resulted in a reduction of intestinal lipocalin-2, an adipokine associated with the development of inflammation and insulin resistance, and higher levels of short-chain fatty acids, which are associated with improved glucose homeostasis and insulin sensitivity as well as modulation of CNS functions, as reported above. |
Formal Description Interaction-ID: 77577 |
environment vegetarian diet increases_quantity of drug/chemical compound Short-chain fatty acid |
Comment | In particular, oleuropein aglycone and oleocanthal, two phenolic components of extra virgin olive oil, have been shown to promote Abeta clearance and autophagy as well as inhibition of tau aggregation and neuroinflammation. |
Formal Description Interaction-ID: 77579 |
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Comment | In particular, oleuropein aglycone and oleocanthal, two phenolic components of extra virgin olive oil, have been shown to promote Abeta clearance and autophagy as well as inhibition of tau aggregation and neuroinflammation. |
Formal Description Interaction-ID: 77581 |
drug/chemical compound Oleocanthal increases_activity of process |
Comment | In particular, oleuropein aglycone and oleocanthal, two phenolic components of extra virgin olive oil, have been shown to promote Abeta clearance and autophagy as well as inhibition of tau aggregation and neuroinflammation. |
Formal Description Interaction-ID: 77582 |
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Comment | In particular, oleuropein aglycone and oleocanthal, two phenolic components of extra virgin olive oil, have been shown to promote Abeta clearance and autophagy as well as inhibition of tau aggregation and neuroinflammation. |
Formal Description Interaction-ID: 77583 |
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Comment | In particular, oleuropein aglycone and oleocanthal, two phenolic components of extra virgin olive oil, have been shown to promote Abeta clearance and autophagy as well as inhibition of tau aggregation and neuroinflammation. |
Formal Description Interaction-ID: 77584 |
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Comment | In particular, oleuropein aglycone and oleocanthal, two phenolic components of extra virgin olive oil, have been shown to promote Abeta clearance and autophagy as well as inhibition of tau aggregation and neuroinflammation. |
Formal Description Interaction-ID: 77585 |
drug/chemical compound Oleuropein aglycone decreases_quantity of phenotype MAPT aggregation |
Comment | In particular, oleuropein aglycone and oleocanthal, two phenolic components of extra virgin olive oil, have been shown to promote Abeta clearance and autophagy as well as inhibition of tau aggregation and neuroinflammation. |
Formal Description Interaction-ID: 77586 |
drug/chemical compound Oleocanthal decreases_quantity of phenotype MAPT aggregation |
Comment | In particular, oleuropein aglycone and oleocanthal, two phenolic components of extra virgin olive oil, have been shown to promote Abeta clearance and autophagy as well as inhibition of tau aggregation and neuroinflammation. |
Formal Description Interaction-ID: 77587 |
drug/chemical compound Oleuropein aglycone decreases_activity of phenotype neuroinflammation |
Comment | In particular, oleuropein aglycone and oleocanthal, two phenolic components of extra virgin olive oil, have been shown to promote Abeta clearance and autophagy as well as inhibition of tau aggregation and neuroinflammation. |
Formal Description Interaction-ID: 77588 |
drug/chemical compound Oleocanthal decreases_activity of phenotype neuroinflammation |
Comment | Oleocanthal has been found to stimulate Abeta clearance by upregulating two major transporters of Abeta expressed in the blood‚Äďbrain barrier (ie,P-glycoprotein and low-density lipoprotein receptor-related protein 1), consequently increasing the brain efflux rate, as shown in murine brain endothelial cells in vitro and in C57BL/6 wild-type mice in vivo. |
Formal Description Interaction-ID: 77593 |
drug/chemical compound Oleocanthal increases_expression of gene/protein |
Drugbank entries | Show/Hide entries for LRP1 |
Comment | Tea phenolics and their aromatic metabolites have been reported to elicit bacteriostatic or antimicrobial activities on gut microbiota, specifically inhibiting the growth of some pathogenic bacteria (ie, Clostridium perfringens, Clostridium difficile, and Bacteroides species). |
Formal Description Interaction-ID: 77598 |
drug/chemical compound Tea phenolics decreases_quantity of environment Clostridium difficile |
Comment | Tea phenolics and their aromatic metabolites have been reported to elicit bacteriostatic or antimicrobial activities on gut microbiota, specifically inhibiting the growth of some pathogenic bacteria (ie, Clostridium perfringens, Clostridium difficile, and Bacteroides species). |
Formal Description Interaction-ID: 77600 |
drug/chemical compound Tea phenolics decreases_quantity of environment Bacteroides |
Comment | Probiotics and prebiotics can stimulate the growth of Bifidobacterium populations while concomitantly decreasing the growth of enterobacteria. |
Formal Description Interaction-ID: 97594 |
environment Probiotics increases_quantity of environment Bifidobacterium |
Comment | Probiotics and prebiotics can stimulate the growth of Bifidobacterium populations while concomitantly decreasing the growth of enterobacteria. |
Formal Description Interaction-ID: 97595 |
environment prebiotic diet increases_quantity of environment Probiotics |
Comment | Probiotics and prebiotics can stimulate the growth of Bifidobacterium populations while concomitantly decreasing the growth of enterobacteria. |
Formal Description Interaction-ID: 97601 |
environment prebiotic diet increases_activity of environment Probiotics |
Comment | A clinical intervention trial involving 6 obese subjects with type 2 diabetes and/or hypertension who followed a strict vegetarian diet for 1 month showed that the vegetarian diet promoted a reduction of gut inflammation, with a decrease of pathobionts (ie, Enterobacteriaceae) and an increase of commensal microbes (ie, Bacteroides fragilis and Clostridium species belonging to clusters XIVa and IV). This resulted in a reduction of intestinal lipocalin-2, an adipokine associated with the development of inflammation and insulin resistance, and higher levels of short-chain fatty acids, which are associated with improved glucose homeostasis and insulin sensitivity as well as modulation of CNS functions, as reported above. |
Formal Description Interaction-ID: 125739 |
environment vegetarian diet increases_quantity of environment Clostridium IV |
Comment | Serum amyloid A proteins (Apolipoprotein serum amyloid A), a family of apolipoproteins expressed either constitutively at different levels in different normal human tissues (eg, breast, stomach, small and large intestine, prostate, lung, pancreas, kidney, tonsil, thyroid, pituitary, placenta, skin epidermis, and brain) or in response to inflammatory stimuli, have been found localized within senile plaques in the brains of AD patients. |
Formal Description Interaction-ID: 144042 |
process increases_activity of |
Comment | In vitro treatment with serum amyloid A (Apolipoprotein serum amyloid A) was found to stimulate glial cell reactivity, as shown by the upregulation of several cytokine genes (eg, IL-6, TNF-alpha, IL-12 p40, IL-23 p19, and IL-10) and of inducible nitric oxide synthase, particularly in microglial cells and, to a lesser extent, in astrocytes. |
Formal Description Interaction-ID: 144043 |
gene/protein SAA increases_activity of tissue/cell line |
Comment | Serum amyloid A proteins (Apolipoprotein serum amyloid A), a family of apolipoproteins expressed either constitutively at different levels in different normal human tissues (eg, breast, stomach, small and large intestine, prostate, lung, pancreas, kidney, tonsil, thyroid, pituitary, placenta, skin epidermis, and brain) or in response to inflammatory stimuli, have been found localized within senile plaques in the brains of AD patients. |
Formal Description Interaction-ID: 144044 |
gene/protein SAA is_expressed_in tissue/cell line |
Comment | Serum amyloid A proteins (Apolipoprotein serum amyloid A), a family of apolipoproteins expressed either constitutively at different levels in different normal human tissues (eg, breast, stomach, small and large intestine, prostate, lung, pancreas, kidney, tonsil, thyroid, pituitary, placenta, skin epidermis, and brain) or in response to inflammatory stimuli, have been found localized within senile plaques in the brains of AD patients. |
Formal Description Interaction-ID: 144045 |
gene/protein SAA is_expressed_in tissue/cell line |
Comment | Serum amyloid A proteins (Apolipoprotein serum amyloid A), a family of apolipoproteins expressed either constitutively at different levels in different normal human tissues (eg, breast, stomach, small and large intestine, prostate, lung, pancreas, kidney, tonsil, thyroid, pituitary, placenta, skin epidermis, and brain) or in response to inflammatory stimuli, have been found localized within senile plaques in the brains of AD patients. |
Formal Description Interaction-ID: 144046 |
gene/protein SAA is_expressed_in tissue/cell line |
Comment | Serum amyloid A proteins (Apolipoprotein serum amyloid A), a family of apolipoproteins expressed either constitutively at different levels in different normal human tissues (eg, breast, stomach, small and large intestine, prostate, lung, pancreas, kidney, tonsil, thyroid, pituitary, placenta, skin epidermis, and brain) or in response to inflammatory stimuli, have been found localized within senile plaques in the brains of AD patients. |
Formal Description Interaction-ID: 144047 |
gene/protein SAA is_expressed_in tissue/cell line |
Comment | Serum amyloid A proteins (Apolipoprotein serum amyloid A), a family of apolipoproteins expressed either constitutively at different levels in different normal human tissues (eg, breast, stomach, small and large intestine, prostate, lung, pancreas, kidney, tonsil, thyroid, pituitary, placenta, skin epidermis, and brain) or in response to inflammatory stimuli, have been found localized within senile plaques in the brains of AD patients. |
Formal Description Interaction-ID: 144048 |
gene/protein SAA is_expressed_in tissue/cell line |
Comment | Serum amyloid A proteins (Apolipoprotein serum amyloid A), a family of apolipoproteins expressed either constitutively at different levels in different normal human tissues (eg, breast, stomach, small and large intestine, prostate, lung, pancreas, kidney, tonsil, thyroid, pituitary, placenta, skin epidermis, and brain) or in response to inflammatory stimuli, have been found localized within senile plaques in the brains of AD patients. |
Formal Description Interaction-ID: 144049 |
gene/protein SAA is_expressed_in tissue/cell line |
Comment | Serum amyloid A proteins (Apolipoprotein serum amyloid A), a family of apolipoproteins expressed either constitutively at different levels in different normal human tissues (eg, breast, stomach, small and large intestine, prostate, lung, pancreas, kidney, tonsil, thyroid, pituitary, placenta, skin epidermis, and brain) or in response to inflammatory stimuli, have been found localized within senile plaques in the brains of AD patients. |
Formal Description Interaction-ID: 144050 |
gene/protein SAA is_expressed_in tissue/cell line |
Comment | Serum amyloid A proteins (Apolipoprotein serum amyloid A), a family of apolipoproteins expressed either constitutively at different levels in different normal human tissues (eg, breast, stomach, small and large intestine, prostate, lung, pancreas, kidney, tonsil, thyroid, pituitary, placenta, skin epidermis, and brain) or in response to inflammatory stimuli, have been found localized within senile plaques in the brains of AD patients. |
Formal Description Interaction-ID: 144051 |
gene/protein SAA is_expressed_in tissue/cell line |
Comment | Serum amyloid A proteins (Apolipoprotein serum amyloid A), a family of apolipoproteins expressed either constitutively at different levels in different normal human tissues (eg, breast, stomach, small and large intestine, prostate, lung, pancreas, kidney, tonsil, thyroid, pituitary, placenta, skin epidermis, and brain) or in response to inflammatory stimuli, have been found localized within senile plaques in the brains of AD patients. |
Formal Description Interaction-ID: 144052 |
gene/protein SAA is_expressed_in tissue/cell line |
Comment | Serum amyloid A proteins (Apolipoprotein serum amyloid A), a family of apolipoproteins expressed either constitutively at different levels in different normal human tissues (eg, breast, stomach, small and large intestine, prostate, lung, pancreas, kidney, tonsil, thyroid, pituitary, placenta, skin epidermis, and brain) or in response to inflammatory stimuli, have been found localized within senile plaques in the brains of AD patients. |
Formal Description Interaction-ID: 144053 |
gene/protein SAA is_expressed_in tissue/cell line |
Comment | Serum amyloid A proteins (Apolipoprotein serum amyloid A), a family of apolipoproteins expressed either constitutively at different levels in different normal human tissues (eg, breast, stomach, small and large intestine, prostate, lung, pancreas, kidney, tonsil, thyroid, pituitary, placenta, skin epidermis, and brain) or in response to inflammatory stimuli, have been found localized within senile plaques in the brains of AD patients. |
Formal Description Interaction-ID: 144054 |
gene/protein SAA is_expressed_in tissue/cell line |
Comment | Serum amyloid A proteins (Apolipoprotein serum amyloid A), a family of apolipoproteins expressed either constitutively at different levels in different normal human tissues (eg, breast, stomach, small and large intestine, prostate, lung, pancreas, kidney, tonsil, thyroid, pituitary, placenta, skin epidermis, and brain) or in response to inflammatory stimuli, have been found localized within senile plaques in the brains of AD patients. |
Formal Description Interaction-ID: 144055 |
gene/protein SAA is_expressed_in tissue/cell line |
Comment | Serum amyloid A proteins (Apolipoprotein serum amyloid A), a family of apolipoproteins expressed either constitutively at different levels in different normal human tissues (eg, breast, stomach, small and large intestine, prostate, lung, pancreas, kidney, tonsil, thyroid, pituitary, placenta, skin epidermis, and brain) or in response to inflammatory stimuli, have been found localized within senile plaques in the brains of AD patients. |
Formal Description Interaction-ID: 144056 |
gene/protein SAA is_expressed_in tissue/cell line |
Comment | Serum amyloid A proteins (Apolipoprotein serum amyloid A), a family of apolipoproteins expressed either constitutively at different levels in different normal human tissues (eg, breast, stomach, small and large intestine, prostate, lung, pancreas, kidney, tonsil, thyroid, pituitary, placenta, skin epidermis, and brain) or in response to inflammatory stimuli, have been found localized within senile plaques in the brains of AD patients. |
Formal Description Interaction-ID: 144057 |
gene/protein SAA is_expressed_in tissue/cell line |
Comment | Serum amyloid A proteins (Apolipoprotein serum amyloid A), a family of apolipoproteins expressed either constitutively at different levels in different normal human tissues (eg, breast, stomach, small and large intestine, prostate, lung, pancreas, kidney, tonsil, thyroid, pituitary, placenta, skin epidermis, and brain) or in response to inflammatory stimuli, have been found localized within senile plaques in the brains of AD patients. |
Formal Description Interaction-ID: 144058 |
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Comment | It has been shown that bacteria populating the gut microbiota can release significant amounts of amyloids and lipopolysaccharides, which might play a role in the modulation of signaling pathways and the production of proinflammatory cytokines related to the pathogenesis of Alzheimer disease. Additionally, nutrients have been shown to affect the composition of the gut microbiota as well as the formation and aggregation of cerebral amyloid-beta. |
Formal Description Interaction-ID: 144059 |
environment gut microbiota increases_quantity of gene/protein Amyloid proteins, microbial |
Comment | Amyloid brain influx through the blood‚Äďbrain barrier is known to be mediated by the receptor for advanced glycosylation products (RAGE) and is dependent on amyloid chaperones and apolipoproteins E and J, while amyloid clearance is controlled by the low-density lipoprotein receptor-related protein 1. These transportation mechanisms are known to be altered in AD patients. |
Formal Description Interaction-ID: 144060 |
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Comment | Nutrients have been shown to affect the composition of the gut microbiota as well as the formation and aggregation of cerebral amyloid-beta. |
Formal Description Interaction-ID: 144061 |
environment nutrients affects_quantity of environment gut microbiota |
Comment | Escherichia coli, Salmonella enterica, Salmonella typhimurium, Bacillus subtilis, Mycobacterium tuberculosis, and Staphylococcus aureus are some of the many bacterial strains that produce functional extracellular amyloid fibers. These bacteria might interact with the host environment in multiple ways. In particular, the E. coli endotoxin was found to potentiate the formation of Abeta fibrils in vitro and, for this reason, might be implicated in the pathogenesis of AD. |
Formal Description Interaction-ID: 144062 |
environment Escherichia coli increases_quantity of phenotype |