Parkinson's Disease and Systemic Inflammation

Abstract

Peripheral inflammation triggers exacerbation in the central brain's ongoing damage in several neurodegenerative diseases. Systemic inflammatory stimulus induce a general response known as sickness behaviour, indicating that a peripheral stimulus can induce the synthesis of cytokines in the brain. In Parkinson's disease (PD), inflammation was mainly associated with microglia activation that can underlie the neurodegeneration of neurons in the substantia nigra (SN). Peripheral inflammation can transform the “primed” microglia into an “active” state, which can trigger stronger responses dealing with neurodegenerative processes. Numerous evidences show that systemic inflammatory processes exacerbate ongoing neurodegeneration in PD patient and animal models. Anti-inflammatory treatment in PD patients exerts a neuroprotective effect. In the present paper, we analyse the effect of peripheral infections in the etiology and progression in PD patients and animal models, suggesting that these peripheral immune challenges can exacerbate the symptoms in the disease.

Cited by papers we hold 8

• Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets · 2023
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• Inflammation in Parkinson’s Disease: Mechanisms and Therapeutic Implications · 2020
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• Designer exosomes produced by implanted cells intracerebrally deliver therapeutic cargo for Parkinson’s disease treatment · 2018
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• Brain and Peripheral Atypical Inflammatory Mediators Potentiate Neuroinflammation and Neurodegeneration · 2017
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• Decrease of gene expression of astrocytic 5-HT2B receptor parallels development of anhedonia in a mouse model of Parkinson’s disease · 2015
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• The many roads to mitochondrial dysfunction in neuroimmune and neuropsychiatric disorders · 2015
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• Central pathways causing fatigue in neuro-inflammatory and autoimmune illnesses · 2015
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• The PPAR-γ agonist pioglitazone modulates inflammation and induces neuroprotection in parkinsonian monkeys · 2011
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