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Updated: Mar 24, 2026
Modeling Amyloid-β42 Toxicity and Neurodegeneration in Adult Zebrafish Brain
Published on: October 25, 2017
Zebrafish study provides evidence for Porphyromonas gingivalis outer membrane vesicles eliciting Alzheimer's
Jianbin Guo1, Kaijin Lin1,2, Ruiyun Liang1,2
1Clinical Research Center for Oral Tissue Deficiency Diseases of Fujian Province & Fujian Key Laboratory of Oral Diseases & Fujian Provincial Engineering Research Center of Oral Biomaterial, School and Hospital of Stomatology, Fujian Medical University, Fuzhou, China.
Introduction:
Periodontitis has been epidemiologically linked to an increased risk of Alzheimer's disease (AD), yet the mechanistic contribution of periodontal pathogens remains insufficiently understood. Building on our previous findings that Porphyromonas gingivalis outer membrane vesicles (OMVs) induce cardiovascular dysfunction, this study investigates whether these vesicles also drive AD-related pathology using the zebrafish model.
Methods:
We microinjected P. gingivalis OMVs into the common cardinal vein of zebrafish larvae to evaluate locomotor behavior, brain injury, and neuroinflammatory responses. Integrated proteomic and transcriptomic analyses were performed to identify alterations in AD-associated pathways, and acetylcholinesterase activity along with Aβ1-42 plaque accumulation were quantified to validate hallmark AD phenotypes.
Results:
OMV exposure resulted in significant neurotoxicity, locomotor deficits, and robust neuroinflammation, accompanied by pronounced dysregulation of AD-related molecular pathways. Notably, OMVs markedly increased acetylcholinesterase activity and promoted Aβ1-42 deposition in larval brains.
Discussion:
These findings demonstrate that P. gingivalis OMVs act as potent inducers of neuronal damage and AD-like pathological features in vivo, providing mechanistic insight into how periodontal pathogens may contribute to neurodegenerative disease progression.
