Aspects of Innate Immunity and Parkinson’s Disease

Huang, Yue; Halliday, Glenda M.

doi:10.3389/fphar.2012.00033

Cited by 19 publications

(15 citation statements)

References 123 publications

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“…It is known that patients with PD have inadequate innate immune responses, increased markers of adaptive immunity, and disruption of the blood brain barrier. 45 This makes a common underlying immunologic association between PD and melanoma plausible.…”

Section: Discussionmentioning

confidence: 99%

Parkinson Disease and Melanoma

Dalvin

Damento

Yawn

et al. 2017

Mayo Clinic Proceedings

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Objective To examine an association between melanoma and Parkinson’s disease (PD). Patients and Methods (Phase I) Rochester Epidemiology Project (REP) records were used to identify PD patients in Olmsted County, MN (1/1/1976–12/31/2013), with three matched controls per case. Following review, JMP statistical software with logistic regression analysis was used to assess risk of prior history of melanoma in PD patients versus controls. (Phase II) All REP cases of melanoma were identified (1/1/1976–12/31/2014), with one control each. A Cox proportional hazards model was used to assess risk of developing PD post-index date in cases versus controls, and Kaplan-Meier analysis was performed to determine 35-year cumulative risk of PD. A Cox proportional hazards model was used to calculate risk of death from metastatic melanoma in melanoma patients without PD compared to those with PD. Results (Phase I) PD subjects had a 3.8-fold increased probability of having pre-existing melanoma compared to controls (CI 2.1–6.8, P<.001). (Phase II) Melanoma patients had a 4.2-fold increased risk of developing PD (CI 2.0–8.8, P<.001). Kaplan-Meier analysis revealed an increased 35-year cumulative risk of PD in melanoma patients (11.8%) compared to controls (2.6%), P<.001. Melanoma patients without PD had a 10.5-fold increased relative risk of dying from metastatic melanoma compared to melanoma patients with PD (CI 1.5–72.2, P=.02). Conclusion There appears to be an association between melanoma and PD. Further study is warranted; but based on these results, physicians may consider counseling melanoma patients regarding PD risk and implementing cutaneous and ocular melanoma surveillance in PD patients.

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Section: Discussionmentioning

confidence: 99%

Parkinson Disease and Melanoma

Dalvin

Damento

Yawn

et al. 2017

Mayo Clinic Proceedings

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“…Several GO terms related to immunity are also found in common in L-DOPA and L-DOPA/HFS and never found after HFS alone. Increasing evidence support the involvement of innate and adaptive immunity in PD progression [81]; altered immune system in PD might in part be linked to an immunoregulatory role of dopamine [82]. Whether the expression of LIDs might involve an abnormal immune response then deserves further investigation.…”

Section: Discussionmentioning

confidence: 99%

Striatal Molecular Signature of Subchronic Subthalamic Nucleus High Frequency Stimulation in Parkinsonian Rat

et al. 2013

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This study addresses the molecular mechanisms underlying the action of subthalamic nucleus high frequency stimulation (STN-HFS) in the treatment of Parkinson's disease and its interaction with levodopa (L-DOPA), focusing on the striatum. Striatal gene expression profile was assessed in rats with nigral dopamine neuron lesion, either treated or not, using agilent microarrays and qPCR verification. The treatments consisted in anti-akinetic STN-HFS (5 days), chronic L-DOPA treatment inducing dyskinesia (LIDs) or the combination of the two treatments that exacerbated LIDs. STN-HFS modulated 71 striatal genes. The main biological processes associated with the differentially expressed gene products include regulation of growth, of apoptosis and of synaptic transmission, and extracellular region is a major cellular component implicated. In particular, several of these genes have been shown to support survival or differentiation of striatal or of dopaminergic neurons. These results indicate that STN HFS may induce widespread anatomo-functional rearrangements in the striatum and create a molecular environment favorable for neuroprotection and neuroplasticity. STN-HFS and L-DOPA treatment share very few common gene regulation features indicating that the molecular substrates underlying their striatal action are mostly different; among the common effects is the down-regulation of Adrb1, which encodes the adrenergic beta-1- receptor, supporting a major role of this receptor in Parkinson's disease. In addition to genes already reported to be associated with LIDs (preprodynorphin, thyrotropin-releasing hormone, metabotropic glutamate receptor 4, cannabinoid receptor 1), the comparison between DOPA and DOPA/HFS identifies immunity-related genes as potential players in L-DOPA side effects.

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“…106–109 Currently there are very few studies exploring the relationship between exercise and the immune system in individuals with PD. Yet it is well recognized that there is a strong immune component in PD 110 . Reports have shown that exercise (cycling) can increase plasma levels of the anti-inflammatory cytokine IL-10 in individuals with PD along with improved motor performance.…”

Section: Exercise and Parkinson’s Diseasementioning

confidence: 99%

Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson's disease

Petzinger

Fisher

McEwen

et al. 2013

The Lancet Neurology

606

456

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The purpose of this review is to highlight the potential role of exercise in promoting neuroplasticity and repair in Parkinson’s disease (PD). Exercise interventions in individuals with PD incorporate goal-based motor skill training in order to engage cognitive circuitry important in motor learning. Using this exercise approach, physical therapy facilitates learning through instruction and feedback (reinforcement), and encouragement to perform beyond self-perceived capability. Individuals with PD become more cognitively engaged with the practice and learning of movements and skills that were previously automatic and unconscious. Studies that have incorporated both goal-based training and aerobic exercise have supported the potential for improving both cognitive and automatic components of motor control. Utilizing animal models, basic research is beginning to reveal exercise-induced effects on neuroplasticity. Since neuroplasticity occurs at the level of circuits and synaptic connections, we examine the effects of exercise from this perspective.

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Aspects of Innate Immunity and Parkinson’s Disease

Cited by 19 publications

References 123 publications

Parkinson Disease and Melanoma

Parkinson Disease and Melanoma

Striatal Molecular Signature of Subchronic Subthalamic Nucleus High Frequency Stimulation in Parkinsonian Rat

Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson's disease

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