ArticleCellular and molecular life sciences : CMLS2023
Amyloid-β mediates intestinal dysfunction and enteric neurons loss in Alzheimer's disease transgenic mouse.
Article in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- Polymeric alpha-1 antitrypsin perturbs Paneth cell proteostasis and exacerbates intestinal inflammation.Signal transduction and targeted therapy · 2026Article
- The short-chain fatty acid butyrate prevents gut-brain amyloid-β pathology and neuroinflammation in an Alzheimer mouse model.Molecular psychiatry · 2026Article
- Article
- Dexmedetomidine Exerts Multi-level Effects to Ameliorate Alzheimer's Disease Pathology in the Adult Zebrafish Brain.Molecular neurobiology · 2026Article
- Role of mitochondria in neuronal function and survival in the enteric and central nervous systems.Cellular and molecular life sciences : CMLS · 2026Review
- Comparison of amyloid and tau pathology in the small and large intestines of individuals with Alzheimer's disease, Parkinson's disease, and Dementia with Lewy bodies.microPublication biology · 2026Article
- Interruption of the Gut Integrity Contributes to Early Accumulation of Amyloid-β in the Enteric Nervous System in Rats Supplemented with a High-Fat Diet.Molecular neurobiology · 2025Article
- Immune, blood-brain barrier, and metabolic biomarkers mediate gut-brain axis crosstalk in alzheimer's disease.Biomarker research · 2025Article
- [18F]flutemetamol uptake in the colon of a memory clinic population and its association with brain amyloidosis and the gut microbiota profile: an exploratory study.European journal of nuclear medicine and molecular imaging · 2025Article
- Studying the Role of Myenteric Amyloidosis in Gastrointestinal Dysmotility and Enteric Neural Dysfunction Using APP/PS1 Mice-Is It an Adequate Animal Model?Neurogastroenterology and motility · 2025Article
- Gastrointestinal Dysfunction and Low-Grade Inflammation Associate With Enteric Neuronal Amyloid-β in a Model for Amyloid Pathology.Neurogastroenterology and motility · 2025Article
- Article
- Shattering the Amyloid Illusion: The Microbial Enigma of Alzheimer's Disease Pathogenesis-From Gut Microbiota and Viruses to Brain Biofilms.Microorganisms · 2025Review
- Mechanisms of action and applications ofFrontiers in pharmacology · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is traditionally considered as a brain disorder featured by amyloid-β (Aβ) deposition. The current study on whether pathological changes of AD extend to the enteric nervous system (ENS) is still in its infancy. In this study, we found enteric Aβ deposition, intestinal dysfunction, and colonic inflammation in the young APP/PS1 mice. Moreover, these mice exhibited cholinergic and nitrergic signaling pathways damages and enteric neuronal loss. Our data show that Aβ42 treatment remarkably affected the gene expression of cultured myenteric neurons and the spontaneous contraction of intestinal smooth muscles. The intra-colon administration of Aβ42 induced ENS dysfunction, brain gliosis, and β-amyloidosis-like changes in the wild-type mice. Our results suggest that ENS mirrors the neuropathology observed in AD brains, and intestinal pathological changes may represent the prodromal events, which contribute to brain pathology in AD. In summary, our findings provide new opportunities for AD early diagnosis and prevention.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.