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In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
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Outer membrane vesicles enhance tau phosphorylation and contribute to cognitive impairment

Shouchao Wei1, Wanjuan Peng1, Yingren Mai1

  • 1Department of Neurology, Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Institute of Neurology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.

Journal of Cellular Physiology
|October 31, 2019
PubMed

Insights

Gut bacteria outer membrane vesicles (OMVs) disrupt the blood-brain barrier, triggering inflammation and tau phosphorylation. This leads to cognitive impairment, suggesting a link between gut microbiota and Alzheimer's disease pathology.

Area of Science:

  • Neuroscience
  • Microbiology
  • Immunology

Background:

  • Gut microbiota (GM) is implicated in Alzheimer's disease (AD) pathogenesis.
  • Outer membrane vesicles (OMVs) are produced by GM, but their role in AD is unclear.
  • Blood-brain barrier (BBB) disruption is a key factor in AD.

Purpose of the Study:

  • To investigate the role of OMVs in cognitive dysfunction.
  • To elucidate the mechanism by which OMVs affect the brain.
  • To determine if OMVs contribute to AD-related pathology.

Main Methods:

  • Induction of BBB disruption and administration of OMVs.
  • Assessment of cognitive function (learning and memory).
  • Analysis of tau phosphorylation, glial cell activation, and inflammatory cytokine levels in the hippocampus.

Main Results:

  • OMVs were shown to induce cognitive dysfunction following BBB disruption.
  • OMVs promoted tau phosphorylation by activating glycogen synthase kinase 3β (GSK-3β).
  • OMVs activated astrocytes and microglia, increasing inflammatory cytokine secretion in the hippocampus.

Conclusions:

  • OMVs increase BBB permeability and promote neuroinflammation.
  • OMVs activate the GSK-3β pathway, leading to tau hyperphosphorylation.
  • OMVs derived from gut microbiota contribute to cognitive impairment and AD pathology.
Keywords:
Alzheimer's diseaseastrocytesblood-brain barrierglycogen synthase kinase 3βgut microbiotainflammatory cytokinesinterleukin-1βmicroglianuclear factor κBouter membrane vesiclestautumour necrosis factor-α

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