# Unraveling the Link Between Mitochondrial Dynamics and Neuroinflammation

## TL;DR

This paper explores how mitochondrial dynamics influence neuroinflammation and their role in neurodegenerative diseases like Parkinson's and Alzheimer's.

## Contribution

The paper highlights novel connections between mitochondrial dysfunction and immune responses in central nervous system diseases.

## Key findings

- Mitochondrial Ca2+ homeostasis alterations induce innate immune pathways linked to neuroinflammation.
- Regulating mitochondrial dynamics reduces oxidative stress and promotes cell viability in CNS diseases.
- Mitochondrial DNA and mtROS contribute to type I IFN responses and neurodegeneration.

## Abstract

Neuroinflammatory and neurodegenerative diseases are a major public health problem worldwide, especially with the increase of life-expectancy observed during the last decades. For many of these diseases, we still lack a full understanding of their etiology and pathophysiology. Nonetheless their association with mitochondrial dysfunction highlights this organelle as an important player during CNS homeostasis and disease. Markers of Parkinson (PD) and Alzheimer (AD) diseases are able to induce innate immune pathways induced by alterations in mitochondrial Ca2+ homeostasis leading to neuroinflammation. Additionally, exacerbated type I IFN responses triggered by mitochondrial DNA (mtDNA), failures in mitophagy, ER-mitochondria communication and mtROS production promote neurodegeneration. On the other hand, regulation of mitochondrial dynamics is essential for CNS health maintenance and leading to the induction of IL-10 and reduction of TNF-α secretion, increased cell viability and diminished cell injury in addition to reduced oxidative stress. Thus, although previously solely seen as power suppliers to organelles and molecular processes, it is now well established that mitochondria have many other important roles, including during immune responses. Here, we discuss the importance of these mitochondrial dynamics during neuroinflammation, and how they correlate either with the amelioration or worsening of CNS disease.