Research
Print page Print page
Switch language
The Capital Region of Denmark - a part of Copenhagen University Hospital
Published

Inflammatory Bowel Diseases and Parkinson's Disease

Research output: Contribution to journalReviewResearchpeer-review

DOI

  1. The Effects of Computer-Based Cognitive Rehabilitation on Working Memory in Patients with Parkinson's Disease: A Systematic Review

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Prepulse Inhibition is Associated with Attention, Processing Speed, and 123-FP-CIT SPECT in Parkinson's disease

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Prepulse Inhibition is Associated with Attention, Processing Speed, and 123I-FP-CIT SPECT in Parkinson's Disease

    Research output: Contribution to journalJournal articleResearchpeer-review

  4. The use of antidepressant medication in Parkinson's disease patients is not affected by the type of antiparkinson medication

    Research output: Contribution to journalJournal articleResearchpeer-review

  1. TDP-43-specific Autoantibody Decline in Patients With Amyotrophic Lateral Sclerosis

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Author Correction: Assessment of brain reference genes for RT-qPCR studies in neurodegenerative diseases

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Epigenetic modulation of AREL1 and increased HLA expression in brains of multiple system atrophy patients

    Research output: Contribution to journalJournal articleResearchpeer-review

  4. Distinct Autoimmune Anti-α-Synuclein Antibody Patterns in Multiple System Atrophy and Parkinson’s Disease

    Research output: Contribution to journalJournal articleResearchpeer-review

View graph of relations

The etiology of Parkinson's disease (PD) is multifactorial, with genetics, aging, and environmental agents all a part of the PD pathogenesis. Widespread aggregation of the α-synuclein protein in the form of Lewy bodies and Lewy neurites, and degeneration of substantia nigra dopamine neurons are the pathological hallmarks of PD. Inflammatory responses manifested by glial reactions, T cell infiltration, and increased expression of inflammatory cytokines, as well as other toxic mediators derived from activated glial cells, are currently recognized as prominent features of PD. Experimental, clinical and epidemiological data suggest that intestinal inflammation contributes to the pathogenesis of PD, and the increasing number of studies suggests that the condition may start in the gastrointestinal system years before any motor symptoms develop. Patients with inflammatory bowel disease (IBD) have a higher risk of developing PD compared with non-IBD individuals. Gene association study has found a genetic link between IBD and PD, and an evidence from animal studies suggests that gut inflammation, similar to that observed in IBD, may induce loss of dopaminergic neurons. Based on preclinical models of PD, it is suggested that the enteric microbiome changes early in PD, and gut infections trigger α-synuclein release and aggregation. In this paper, the possible link between IBD and PD is reviewed based on the available literature. Given the potentially critical role of gastrointestinal pathology in PD pathogenesis, there is reason to suspect that IBD or its treatments may impact PD risk. Thus, clinicians should be aware of PD symptoms in IBD patients.

Original languageEnglish
JournalJournal of Parkinson's Disease
Volume9
Issue numbers2
Pages (from-to)S331-S344
ISSN1877-7171
DOIs
Publication statusPublished - 1 Jan 2019

    Research areas

  • Crohn's disease, Parkinson's disease, brain-gut axis, enteric nervous system, gastrointestinal track inflammation, inflammation, inflammatory bowel disease, ulcerative colitis

ID: 58137928