CARD15 variants in patients with sporadic Parkinson's disease

Białecka, Monika; Kurzawski, Mateusz; Kłodowska-Duda, Gabriela; Opala, Grzegorz; Juźwiak, S.; Kurzawski, Grzegorz; Tan, Eng‐King; Droździk, Marek

doi:10.1016/j.neures.2006.11.012

Cited by 72 publications

(46 citation statements)

References 26 publications

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“…Gut inflammation is hypothesized to play a role in the development of sporadic PD. Overrepresentation of CARD15 mutations associated with Crohn's disease and Helicobacter pylori seropositivity before age 75 in people with sporadic PD supports this hypothesis [90, 91]. A GWAS identified polymorphism in the LRRK2 gene is associated with Crohn's disease.…”

Section: Engagement Of Adaptive Immunity: Microglial Activation and Mmentioning

confidence: 97%

The Role of Innate and Adaptive Immunity in Parkinson's Disease

Kannarkat

Boss

Tansey

2013

Journal of Parkinson's Disease

278

201

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In recent years, inflammation has become implicated as a major pathogenic factor in the onset and progression of Parkinson's disease. Understanding the precise role for inflammation in PD will likely lead to understanding of how sporadic disease arises. In vivo evidence for inflammation in PD includes microglial activation, increased expression of inflammatory genes in the periphery and in the central nervous system (CNS), infiltration of peripheral immune cells into the CNS, and altered composition and phenotype of peripheral immune cells. These findings are recapitulated in various animal models of PD and are reviewed herein. Furthermore, we examine the potential relevance of PD-linked genetic mutations to altered immune function and the extent to which environmental exposures that recapitulate these phenotypes, which may lead to sporadic PD through similar mechanisms. Given the implications of immune system involvement on disease progression, we conclude by reviewing the evidence supporting the potential efficacy of immunomodulatory therapies in PD prevention or treatment. There is a clear need for additional research to clarify the role of immunity and inflammation in this chronic, neurodegenerative disease.

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Section: Engagement Of Adaptive Immunity: Microglial Activation and Mmentioning

confidence: 97%

The Role of Innate and Adaptive Immunity in Parkinson's Disease

Kannarkat

Boss

Tansey

2013

Journal of Parkinson's Disease

278

201

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“…Indeed, polymorphisms in the nucleotide-binding oligiomerization domain 2 (NOD2) gene associated with Crohn's disease, a chronic inflammatory bowel disease, have been shown to be over-represented in patients with idiopathic PD (Bialecka et al, 2007).…”

Section: Epidemiological Evidencementioning

confidence: 99%

Contributions of central and systemic inflammation to the pathophysiology of Parkinson's disease

Collins¹,

Toulouse²,

Connor³

et al. 2012

Neuropharmacology

256

153

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“…At least one of these same variants is also over-represented in PD patients. 100 A recent study suggests that the overlap between CD and PD risk loci extends beyond these known shared associations, 101 so there may be even greater similarity in genetic predisposition to this intestinal inflammatory and this neurodegenerative disorder.…”

Section: Introductionmentioning

confidence: 99%

The gut-brain axis: is intestinal inflammation a silent driver of Parkinson’s disease pathogenesis?

Houser

Tansey

2017

npj Parkinson's Disease

443

348

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The state of the intestinal environment can have profound effects on the activity of the central nervous system through the physiological contributions of the microbiota, regulation of intestinal barrier function, and altered activity of peripheral neurons. The common language employed for much of the gut-brain communication is the modulation of immune activity. Chronic proinflammatory immune activity is increasingly being recognized as a fundamental element of neurodegenerative disorders, and in Parkinson’s disease, inflammation in the intestine appears particularly relevant in pathogenesis. We review the evidence that intestinal dysfunction is present in Parkinson’s disease and that it may reflect the earliest manifestations of Parkinson’s disease pathology, and we link these findings to dysregulated immune activity. Based on this, we present a model for Parkinson’s disease pathogenesis in which the disorder originates in the intestine and progresses with inflammation as its underlying mechanism. More in-depth investigations into the physiological mechanisms underlying peripheral pre-motor symptoms in Parkinson’s disease are expected to lead to the development of novel diagnostic and therapeutic measures that can slow or limit progression of the disease to more advanced stages involving debilitating motor and cognitive symptoms.

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CARD15 variants in patients with sporadic Parkinson's disease

Cited by 72 publications

References 26 publications

The Role of Innate and Adaptive Immunity in Parkinson's Disease

The Role of Innate and Adaptive Immunity in Parkinson's Disease

Contributions of central and systemic inflammation to the pathophysiology of Parkinson's disease

The gut-brain axis: is intestinal inflammation a silent driver of Parkinson’s disease pathogenesis?

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