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Adipose-Derived Mesenchymal Stromal Cells Co-Cultured with Primary Mixed Glia to Reduce Prion-Induced Inflammation

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Pro-inflammatory cytokines modulate glial apolipoprotein E secretion.

Rosanne Aleong¹, Jean-Francois Blain, Judes Poirier

¹Department of Neurology and Neurosurgery, Montreal, Quebec, Canada.

Current Alzheimer Research

|February 22, 2008

Summary

Alzheimer's disease involves immune responses and apolipoprotein E (apoE) gene risk. Interleukin-1beta increased apoE, while tumor necrosis factor-alpha decreased it in rat glial cells, suggesting cytokine roles in AD.

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Adipose-Derived Mesenchymal Stromal Cells Co-Cultured with Primary Mixed Glia to Reduce Prion-Induced Inflammation

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A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes

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Published on: February 5, 2018

Area of Science:

Neuroscience
Immunology
Genetics

Background:

Alzheimer's disease (AD) is linked to neuroinflammation, characterized by elevated cytokines like interleukin (IL)-1 and tumor necrosis factor (TNF)-alpha.
Genetic variants in IL-1 and TNF-alpha, and the apolipoprotein E (apoE) gene (specifically epsilon4), are established risk factors for AD.
Lower brain apoE levels are observed in AD patients carrying the apoE epsilon4 risk allele.

Purpose of the Study:

To investigate the direct effects of IL-1beta and TNF-alpha on apolipoprotein E (apoE) expression in glial cells.
To explore the relationship between inflammatory cytokines and apoE regulation in the context of Alzheimer's disease.

Main Methods:

Primary rat mixed glial cell cultures were treated with IL-1beta and TNF-alpha.
Extracellular apoE protein levels were measured following cytokine treatment.
Primary rat astrocyte cultures were also utilized to assess specific cell type responses.

Main Results:

Treatment with IL-1beta significantly increased extracellular apoE protein levels in mixed glial cell cultures.
Treatment with TNF-alpha significantly reduced extracellular apoE protein levels in both astrocyte and mixed glial cell cultures.
These findings indicate differential regulation of apoE by key inflammatory cytokines.

Conclusions:

Elevated IL-1beta expression may promote apoE production, potentially influencing neuronal remodeling in AD.
Elevated TNF-alpha expression may suppress apoE production, impacting neuronal support and repair mechanisms in AD.
Cytokine-mediated modulation of apoE represents a significant pathway in Alzheimer's disease pathogenesis and neuroinflammation.