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Related Experiment Video

Updated: Jul 29, 2025

Improved 3D Hydrogel Cultures of Primary Glial Cells for In Vitro Modelling of Neuroinflammation

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STING-Triggered CNS Inflammation in Human Neurodegenerative Diseases.

Alex S Ferecskó^1,2, Miranda J Smallwood², Adrian Moore¹

¹UCB Pharma, Slough SL1 3WE, UK.

|May 27, 2023

Summary

The stimulator of interferon genes (STING) pathway is activated in neurodegenerative diseases, potentially by mitochondrial stress and DNA leakage, suggesting it as a therapeutic target for neuroinflammation.

Keywords:

cGAS cerebral endothelial cells cortical neurons neuroinflammation palmitic acid

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Area of Science:

Neuroscience
Immunology
Cell Biology

Background:

Neuroinflammation is implicated in some neurodegenerative diseases, often triggered by viral nucleic acids leading to type I interferons.
The cGAS-STING pathway, activated by DNA, plays a role in immune responses but its activation in human neurodegenerative diseases is understudied.

Purpose of the Study:

To investigate the activation of the cGAS-STING pathway in human neurodegenerative diseases.
To explore the role of mitochondrial stress and DNA leakage in activating the STING pathway.

Main Methods:

Immunohistochemistry on post-mortem CNS tissue from patients with multiple sclerosis, Alzheimer's, Parkinson's, ALS, and controls.
In vitro studies using human brain endothelial cells stimulated with palmitic acid (a STING agonist) to assess mitochondrial stress and inflammatory markers.

Main Results:

Elevated STING protein levels were found in endothelial cells and neurons in neurodegenerative diseases, particularly associated with protein aggregates.
Palmitic acid stimulation induced mitochondrial stress, cytosolic DNA leakage, and increased levels of TBK-1, pIRF3, cGAS, and ICAM-1 in endothelial cells.

Conclusions:

The cGAS-STING pathway is activated in neural and endothelial cells across multiple neurodegenerative diseases.
Mitochondrial stress and subsequent DNA leakage may activate the STING pathway, contributing to neuroinflammation and offering a potential therapeutic target.