Myeloperoxidase: Bridging the gap in neurodegeneration
•MPO induces hypochlorous acid induced Chlorinative stress.•Myeloperoxidase is a key player in the neurodegeneration.•Increased MPO expression augments neurodegeneration and disease progression. Neurodegenerative conditions present a group of complex disease pathologies mostly due to unknown aetiolo...
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Veröffentlicht in: | Neuroscience and biobehavioral reviews 2016-09, Vol.68, p.611-620 |
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Hauptverfasser: | , |
Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | •MPO induces hypochlorous acid induced Chlorinative stress.•Myeloperoxidase is a key player in the neurodegeneration.•Increased MPO expression augments neurodegeneration and disease progression.
Neurodegenerative conditions present a group of complex disease pathologies mostly due to unknown aetiology resulting in neuronal death and permanent neurological disability. Any undesirable stress to the brain, disrupts homeostatic balance, through a remarkable convergence of pathophysiological changes and immune dysregulation. The crosstalk between inflammatory and oxidative mechanisms results in the release of neurotoxic mediators apparently spearheaded by myeloperoxidase derived from activated microglia, astrocytes, neurons as well as peripheral inflammatory cells. These isolated entities combinedly have the potential to flare up and contribute significantly to neuropathology and disease progression. Recent, clinicopathological evidence support the association of myeloperoxidase and its cytotoxic product, hypochlorous acid in a plethora of neurodegenerative diseases including Alzheimer’s disease, Parkinson’s disease, Amyotrophic lateral sclerosis, Multiple sclerosis, Stroke, Epilepsy etc. But the biochemical and mechanistic insights into myeloperoxidase mediated neuroinflammation and neuronal death is still an uncharted territory. The current review outlines the emerging recognition of myeloperoxidase in neurodegeneration, which may offer novel therapeutic and diagnostic targets for neurodegenerative disorders. |
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ISSN: | 0149-7634 1873-7528 |
DOI: | 10.1016/j.neubiorev.2016.06.031 |