# The cGAS–STING Pathway in Dementia: An Emerging Mechanism of Neuroinflammation

## TL;DR

This review explores how the cGAS-STING pathway contributes to dementia-related neuroinflammation and its potential as a new treatment target.

## Contribution

Highlights the cGAS-STING pathway as a novel mechanism and therapeutic target in dementia.

## Key findings

- The cGAS-STING pathway is linked to chronic neuroinflammation in dementia.
- Targeting this pathway could reduce inflammation and neuronal loss in Alzheimer's disease.
- Emerging research suggests its potential for diagnostic and therapeutic applications.

## Abstract

Dementia is a growing global health concern in aging societies, leading to a progressive decline in cognitive function that severely impairs daily life. Despite the growing burden, effective preventive and therapeutic strategies remain elusive, emphasizing the urgent need for novel interventions. Recent advances underscore the pivotal role of neuroinflammation in dementia pathogenesis, particularly in Alzheimer’s disease (AD). Chronic activation of central nervous system immune cells, particularly microglia, exacerbates neurodegeneration and establishes a self-perpetuating cycle of inflammation and cognitive decline. This review focuses on emerging research exploring the cGAS-STING pathway’s role in dementia, examining its potential as a diagnostic and therapeutic target. The cGAS-STING pathway, integral to innate immune responses, may contribute to the chronic neuroinflammation seen in neurodegenerative diseases. By targeting this pathway, new strategies could mitigate the inflammatory processes that drive neuronal loss, offering a promising avenue for therapeutic development in dementia.