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Cited by 826Gut microbiota and healthAlzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

Brain-Gut-Microbiota Axis in Alzheimer’s Disease

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Kowalski, Karol, Mulak, Agata·2019·Journal of Neurogastroenterology and Motility
DOI 10.5056/jnm18087PMC PMC6326209
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Abstract

Disturbances along the brain-gut-microbiota axis may significantly contribute to the pathogenesis of neurodegenerative disorders. Alzheimer's disease (AD) is the most frequent cause of dementia characterized by a progressive decline in cognitive function associated with the formation of amyloid beta (Aβ) plaques and neurofibrillary tangles. Alterations in the gut microbiota composition induce increased permeability of the gut barrier and immune activation leading to systemic inflammation, which in turn may impair the blood-brain barrier and promote neuroinflammation, neural injury, and ultimately neurodegeneration. Recently, Aβ has also been recognized as an antimicrobial peptide participating in the innate immune response. However, in the dysregulated state, Aβ may reveal harmful properties. Importantly, bacterial amyloids through molecular mimicry may elicit cross-seeding of misfolding and induce microglial priming. The Aβ seeding and propagation may occur at different levels of the brain-gut-microbiota axis. The potential mechanisms of amyloid spreading include neuron-to-neuron or distal neuron spreading, direct blood-brain barrier crossing or via other cells as astrocytes, fibroblasts, microglia, and immune system cells. A growing body of experimental and clinical data confirms a key role of gut dysbiosis and gut microbiota-host interactions in neurodegeneration. The convergence of gut-derived inflammatory response together with aging and poor diet in the elderly contribute to the pathogenesis of AD. Modification of the gut microbiota composition by food-based therapy or by probiotic supplementation may create new preventive and therapeutic options in AD.

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  • The gut has been identified as a peripheral reservoir for Aβ.

    “Furthermore, the immune cells of the peritoneum are of great interest in relation to the gut, which has been identified as a peripheral reservoir for Aβ, and as a conduit of peripheral messengers to the brain via the gut-brain-axis [22, 33].”

    From Alzheimer’s disease-associated protective variant Plcg2-P522R modulates peripheral macrophage function in a sex-dimorphic manner (2024) · cites this paper as [33]

    The Amyloid Plaque Formation > Enteric Nervous System section reports Aβ accumulation in the enteric neurons of APP transgenic mice, supporting the narrower point that Aβ can be present in the gut. It does not identify the gut as a peripheral Aβ reservoir generally. The Bacterial Amyloids section describes gut-microbial amyloids, but distinguishes them from Aβ. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • AD risk alleles may elicit their impact on cognition at least in part by altering the microbiome's contribution to neurophysiology.

    “Collectively, these results suggest that the AppNL-F and AppNL-G-F alleles impact the gut microbiome in ways that link to cognitive performance, and support the hypothesis that AD risk alleles may elicit their impact on cognition at least in part by altering the microbiome’s contribution to neurophysiology49–52.”

    From Integrated analysis of behavioral, epigenetic, and gut microbiome analyses in AppNL-G-F, AppNL-F, and wild type mice (2021) · cites this paper as [51]

    The Introduction identifies APP mutations as a cause of early-onset AD, and the “Gut Microbiota in Animal Models of Alzheimer’s Disease” section reports altered microbiota in APP transgenic mice and microbiota-dependent changes in brain amyloid pathology. These findings support a possible gene–microbiota–brain link, but the review does not establish that AD risk alleles affect cognition by altering the microbiome’s contribution to neurophysiology. No page numbers were provided for these passages. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

  • The AppNL-F and AppNL-G-F alleles impact the gut microbiome in ways that link to cognitive performance.

    “Collectively, these results suggest that the AppNL-F and AppNL-G-F alleles impact the gut microbiome in ways that link to cognitive performance, and support the hypothesis that AD risk alleles may elicit their impact on cognition at least in part by altering the microbiome’s contribution to neurophysiology49–52.”

    From Integrated analysis of behavioral, epigenetic, and gut microbiome analyses in AppNL-G-F, AppNL-F, and wild type mice (2021) · cites this paper as [51]

    The “Gut Microbiota in Animal Models of Alzheimer’s Disease” section reports altered gut microbiota in APP transgenic mice and effects of microbiota on brain amyloid pathology. It does not identify the AppNL-F or AppNL-G-F alleles or establish that microbiome changes associated with those alleles link to cognitive performance. No page number is available in our copy. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • The gut has been identified as a conduit of peripheral messengers to the brain via the gut-brain-axis.

    “Furthermore, the immune cells of the peritoneum are of great interest in relation to the gut, which has been identified as a peripheral reservoir for Aβ, and as a conduit of peripheral messengers to the brain via the gut-brain-axis [22, 33].”

    From Alzheimer’s disease-associated protective variant Plcg2-P522R modulates peripheral macrophage function in a sex-dimorphic manner (2024) · cites this paper as [33]

  • Shotgun metagenomic sequencing, analyzed using AI-enhanced bioinformatics, has revealed functional disruptions in AD-associated microbiomes, including altered lipid metabolism and reduced SCFA biosynthesis capacity.

    “Shotgun metagenomic sequencing, analyzed using AI-enhanced bioinformatics, has revealed functional disruptions in AD-associated microbiomes, including altered lipid metabolism and reduced SCFA biosynthesis capacity214.”

    From Artificial intelligence-driven multi-omics approaches in Alzheimer's disease: Progress, challenges, and future directions (2025) · cites this paper as [214]

    The Clinical Data section reports differences in the composition of AD-associated gut microbiota, but not the functional findings claimed here. Searches for shotgun metagenomic sequencing, AI-enhanced bioinformatics, lipid metabolism, and reduced SCFA biosynthesis found no passage establishing those findings; the Animal Models section mentions SCFAs only in a Parkinson’s disease model. Page numbers were not provided in our copy. (LLM, conf=0.75)

    Experimental — accuracy not yet measured

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Cited by

Sorted by citations

Authors
Kowalski, K., & Mulak, A.
Affiliations
University of Wrocław (PL)
Corresponding author
Mulak, Agata
ORCID
Venue
Journal of Neurogastroenterology and Motility
Publisher
The Korean Society of Neurogastroenterology and Motility
Published
2019-01-30
Volume
25
Issue
1
Pages
48-60
ISSN
  • 2093-0879 (ISSN-L)
  • 2093-0887
DOI
10.5056/jnm18087
PMC
PMC6326209
OpenAlex
W2909041556
Cited by
826
References
19
Citations by year
2026: 97 · 2025: 118 · 2024: 106 · 2023: 100 · 2022: 125 · 2021: 138 · 2020: 100 · 2019: 42
FWCI
8.94
Type
journal article
Language
en
Open access
Licence
cc-by-nc
Locations
  • Journal of Neurogastroenterology and Motility (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Alzheimer's disease, brain-gut-microbiota axis, gut dysbiosis, amyloid-beta, blood-brain barrier, neuroinflammation, intestinal permeability, systemic inflammation, bacterial amyloids, molecular mimicry, amyloid seeding, microglial priming, neurodegeneration, probiotics, dietary therapy, aging

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