| Evidence | Source | Results | Reference |
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CNS inflammation | Human brain | Significant increase in the number of reactive microglia in the substantia nigra of PD patients. | [9, 12] | Coexistence of α-synuclein and activated microglia. | [15] | Higher expression/increased levels of inflammatory mediators in PD brains. | [13, 16–18] | Human CSF samples | Increased levels of IL-1β, IL-2, IL-4, IL-6, TGF-α, free TGF-β1, and total TGF-β2 in the CSF of PD patients. | [30–32] |
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Peripheral inflammation | Serum/plasma samples | Increased levels of IFN-γ, IL-1β, IL-2, IL-3, IL-10, MIF, TNF-α, and its soluble receptors sTNFR1 and sTNFR2 in PD patients samples. | [48–58] | Supernatants from cell cultures | MCP-1, MIP-1α, IL-8, IFN-γ, IL-1β, and TNF-α levels were significantly higher in PD patients. | [65] | Blood leukocytes | PD patients exhibited lower total lymphocyte counts; decrease in the percentage of T (CD3+) and B (CD19+) cells and reduction in T helper (Th, CD4+) lymphocytes; higher percentage of NK cells. | [52, 61, 71–74, 77] |
| Genetic evidence | DNA extracted from brain, blood, or buccal samples | Enhancement in IL-1β 511, IL-6, and TNF-α polymorphisms. | [21–24] |
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Epidemiological evidence | Clinical and population-based studies | NSAIDs use was associated with a lower risk for PD. | [91, 92, 94, 95, 104]. | IFN-α-induced Parkinsonism in chronic hepatitis [67–69]. | [67–69] | The relationship between PD and systemic infections (severe influenza). | [70] |
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