From: The progress of gut microbiome research related to brain disorders
Brain disorders | Dysbiosis of microbiota | Pathological and molecular signature | Potential probiotic-based therapeutics |
---|---|---|---|
Stress and depression | Increase of Faecalibacterium, Alistipes, Ruminococcus [112], Campylobacter jejuni [143] and Firmicutes; decrease of Bacteroidetes [251] | Activation and releasing of HPA [121],VFA [112, 141], serotonin 1A receptor [122]; reduced expression of BDNF [122], GABA receptor [119] | Bifidobacterium infantis [121], Lactobacillus rhamnosus [119], Lactobacillus helveticus, Bifidobacterium longum [142], and other Bifidobacterium strains [143] |
Pain and migraine | Dysfunction of CB2 and TLR7 [160]; inflammatory hypernociception [161]; TNF-α induced chronic migrain e[163] | Lactobacillus, B. infantis 35624 and Lactobacillus farciminis [165, 166], Lactobacillus salivarius UCC433 1[167] | |
Autism spectrum disorders | Decreases of Faecalibacterium species [150], Bifidobacteria species, Akkermansia muciniphila; increase of Lactobacillus, Bacteroides, Prevotella, and Alistipes [145, 151, 152]; alteration of Fusobacteria, Verrucomicrobia and Firmicutes/Bacteroides ratio [11] | Disrupted intestinal epithelial permeability [114], mucosal inflammation [148, 149], reduction of SCFA synthesis [150], mucosal inflammation [148, 149] | Bacteroides fragilis [114], Lactobacillus species and Bifidobacterium species [119, 155] |
Parkinson’s disease | Increase of H.pylori [174], E.coli [179], Ralstonia, Oscillospira and Bacteroides [180]; decrease of Prevotellaceae [181], Blautia, Coprococcus, and Roseburia [180] | Higher frequency of α-synuclein detection [175], dopaminergic neuronal loss [177], bowel inflammation and change of permeability [178, 180] | Multiple probiotics strains (Streptococcus salivarius subsp thermophilus, Enterococcus faecium, Lactobacillus rhamnosus GG, Lactobacillus acidophilus, Lactobacillus plantarum, Lactobacillus paracasei, Lactobacillus delbrueckii subsp bulgaricus, and Bifidobacterium) [182] |
Alzheimer’s disease | Chronic H.pylori infection [193, 194]; increase of E.coli, Salmonella spp, Pseudomonas fluorescens, Klebsiella pneumonia, Staphylococcus aureus, Bacillus subtills, Streptomyces coelicolor [190, 196, 197]; Chlamydia pneumoniae infection [199] | Increased levels of IL-1beta, IL-6, and TNF-alpha [186, 187]; extracellular amyloids such as CsgA, Aβ42, FapC, MccE492, phenol-soluble Modulins, TasA, Chaplins, and β-amyloid exhibit cerebral deposition [190, 192, 196, 197, 199] | Lactobacilli and Bifidobacteria [200, 203]; Lactobacillus fermentum NS9 and Lactobacillus helveticus NS8 [201, 202] |
Amyotrophic lateral sclerosis | Reduced levels of butyrate-producing bacteria, including Butyrivibrio fibrisolvens, Escherichia coli, Oscillibacter, Anaerostipes, and Lachnospira [213]; increase of glucose-metabolizing Dorea [214] | Tetanus and botulinum toxins [210, 211]; “leaky gut” [212]; higher richness of OTUs [215]; reduction of butyrate [216] | Lactobacillus strains [217] |
Multiple sclerosis | Increase of Archaea, Psuedomonas, Haemophilus, Blautia, Dorea [219], and Fusobacteria [225]; decrease of Bacteroidetes phyla, Firmicutes phyla, [218] Parabacteroides, Adlercreutzia, Prevotella [219], Bacteroides and Clostridia [218, 222] | BBB integrity disruption and astrocyte pathogenicity [222]; increasing proinflammatory cell infiltration and impaired Treg function [221]; “leaky gut” [219, 220] | Bifidobacterium and lactic acid-producing bacteria [223, 224]; Bacteroidaceae, Faecalibacterium, Ruminococcus, Lactobacillaceae, and Clostridium [226] |
Atherosclerosis | Lactobacillus rhamnosus and Neisseria polysaccharea, Acidovorax spp. and H. pylori cells [232]; Collinsella [233]; Roseburia and Eubacterium [233] | Carnitine-butyrobetaine-trimethylamine-N-oxide pathway [235]; cause vascular atherosclerosis by affecting lipid and hormonal homeostasis [82, 222]; formation of foam cell by inflammation [236, 237] | L. acidophilus 145, B. longum 91 3[238], L. acidophilus and B. bifidum [239], L. plantarum ZDY04 against TMAO [240] |
Stroke | Increase of Porphyromonas gingivalis [242], Gram-negative bacteria [243], Enterobacter, Megasphaera, Oscillibacter; decrease of Bacteroides, Prevotella and Faecalibacterium [245] | Formation of blood clots and platelet aggregation [244]; decrease of regulatory T cells [241] | Antibiotic administration [241] |
Arteriovenous malformation | Gram-negative bacteria [248] | Macrophage infiltration and cytokine secretion [246]; activate TLR4 [248] | Antibiotic and probiotics treatment are controversial [248,249,250] |