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Review
. 2019 Apr 1:2019:4050796.
doi: 10.1155/2019/4050796. eCollection 2019.

The Role of Mitochondrial Damage-Associated Molecular Patterns in Chronic Neuroinflammation

Ekta Bajwa  1 , Caitlin B Pointer  1 , Andis Klegeris  1
Affiliations
Review

The Role of Mitochondrial Damage-Associated Molecular Patterns in Chronic Neuroinflammation

Ekta Bajwa et al. Mediators Inflamm. .

Abstract

Mitochondrial dysfunction has been established as a common feature of neurodegenerative disorders that contributes to disease pathology by causing impaired cellular energy production. Mitochondrial molecules released into the extracellular space following neuronal damage or death may also play a role in these diseases by acting as signaling molecules called damage-associated molecular patterns (DAMPs). Mitochondrial DAMPs have been shown to initiate proinflammatory immune responses from nonneuronal glial cells, including microglia and astrocytes; thereby, they have the potential to contribute to the chronic neuroinflammation present in these disorders accelerating the degeneration of neurons. In this review, we highlight the mitochondrial DAMPs cytochrome c (CytC), mitochondrial transcription factor A (TFAM), and cardiolipin and explore their potential role in the central nervous system disorders including Alzheimer's disease and Parkinson's disease, which are characterized by neurodegeneration and chronic neuroinflammation.

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Figures

Figure 1
Figure 1
Mitochondrial damage-associated molecular patterns (DAMPs) cytochrome c (CytC), mitochondrial transcription factor A (TFAM), and cardiolipin can be released into the central nervous system (CNS) intercellular space where they regulate microglial phagocytosis and the release of inflammatory mediators by microglia. AD = Alzheimer's disease; PD = Parkinson's disease.
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