Activated Schwann cells and increased inflammatory cytokines IL-1β, IL-6, and TNF-α in patients' sural nerve are lack of tight relationship with specific sensory disturbances in Parkinson's disease.
We found no correlations between cytokines and disease duration suggesting that IL-6 and IL-17A are associated with disease severity rather than disease duration in this cohort, furthermore IL-17A may be involved in the underlying pathophysiology of NMS in PD.
Pretreatment with CUMS for 14 days increased the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-a (TNF-a) in the serum, and increased the expression of NLRP-3, ASC, Casepase-1 in the substantia nigra of PD rats.
To study the association between Parkinson's disease (PD)-related pain and plasma interleukin (IL)‑1, IL‑6, IL‑10, and tumour necrosis factor (TNF)‑α levels.
To understand the potential mechanisms involved in the beneficial effects of aspirin (ASA) in mood disorders, Alzheimer's (AD) and Parkinson's disease (PD), we investigated the effects of ASA on the expression of iron transport proteins transferrin receptor 1 (TfR1), ferroportin 1 (Fpn1), and iron storage protein ferritin light chain (Ft-L) in interleukin-6 (IL-6)-treated PC-12 cells.
The results showed that baicalein treatment improved motor impairments, attenuated brain damage, suppressed the production of proinflammatory cytokines (tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6)), modulated the astrocytes and microglia activation, and blocked the activation of nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signals in rotenone-induced rats of PD.
To assess whether inflammation and microglial activation accompany the onset and the progression of PD-like pathology, we investigated the expression of cytokines (<i>interleukin 1 beta (Il1b), interleukin 6 (Il6)</i>) and microglial/macrophage activation markers (<i>Fc gamma receptor III (Fcgr3), mannose receptor 1 (Mrc1), chitinase-like 3 (Ym1), arginase 1 (Arg 1), triggering receptor expressed on myeloid cells 2 (Trem2)</i>), together with microglial ionized calcium binding adapter molecule 1 (Iba1) and astrocyte glial fibrillary acidic protein (GFAP) immunolabeling, in the substantia nigra (SN) of c-rel<sup>-/-</sup> mice, at premotor (4- and 13-month-old) and motor phases (18-month-old).
In contrast to the previously reported gliogenic effects of activation of the IL-6-signal transducer and activator of transcription 3 (STAT3) axis, this review summarizes recent studies showing that IL-6 activation can be neurogenic and has potential therapeutic applications for the treatment of neurodegenerative diseases such as Parkinson's disease.
For the first time, the multilocus approach by the set-association method has been applied for the analysis of a cluster of five genes [tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), IL-8, IL-1alpha and IL-10] involved in the brain neuroinflammatory pathway in Parkinson's disease (PD), in a well-defined group of 197 PD patients and 173 control subjects from Spain.
Programmed cell death of the nigro-striatal dopamine neurons in PD has been suggested from the following findings on postmortem brains: (1) increased levels of pro-inflammatory cytokines such as TNF-alpha and IL-6; (2) increased levels of apoptosis-related factors such as TNF-alpha receptor R1 (p 55), soluble Fas and bcl-2, and increased activities of caspases 1 and 3; and (3) decreased levels of neurotrophins such as brain-derived nerve growth factor (BDNF).
Our results indicate that the G-174C SNP in the IL-6 promoter may influence the risk for developing PD, particularly regarding early age of onset PD, and that the effect is modified by interaction of the G-1730A SNP in the ERbeta gene.
The increased number of activated microglia and the production of neurotrophic cytokines such as IL-6, together with the decreased expression of the neurotrophic factors of neurons in the hippocampus of PD and DLB brains, may be related to functional cellular changes associated with dementia.
Table 1 Biochemical Alterations in Substantia Nigra of Parkinson's Disease Indicating Oxidative Stress Elevated Decreased Iron (in microglia, astrocytes, oligodendrocytes, and melanized dopamine neurons and mitochondria) GSH (GSSG unchanged); GSH/GSSG ratio decreased Mitochondrial complex I Ferritin Calcium binding protein (calbindin 28) Mitochondrial monoamine oxidase B Transferrin and transferrin receptor Lipofuscin Vitamins E and C Ubiquitin Copper Cu/Zn-superoxide dismutase Cytotoxic cytokines (TNF-a, IL-1, IL-6) Inflammatory transcription factor NFKB Heme oxygenase-1 Ratio of oxidized to reduced glutathione (GSSG/GSH) Nitric oxide Neuromelanin.