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Clinical Trials/NCT01155492
NCT01155492CompletedNot Applicable

Increased Gut Permeability to Lipopolysaccharides (LPS) in Parkinson's Disease

Rush University Medical Center1 site in 1 country43 target enrollmentStarted: September 2007Last updated:
Conditions

Trial Snapshot

Phase
Not Applicable
Status
Completed
Enrollment
43
Locations
1
Primary Endpoint
Total urine sugar per 24 hours

Study Overview

Brief Summary

The gut may be a portal of entry for agents that cause or contribute to the causes of Parkinson's disease (PD). The investigators are studying changes in the normal population of gut flora and in intestinal permeability and their associations with early PD.

Detailed Description

Clinical and pathological data suggest Parkinson's disease (PD) may result from an inflammatory process beginning in the intestinal wall that initiates alpha-synuclein aggregation, which then spreads from neuron to neuron, reaching the central nervous system. Bacteria living within the intestinal tract produce lipopolysaccharide endotoxin, a toxin known to induce parkinsonism in animal models. We hypothesize that exposure to LPS, either from excessive production or excessive absorption may be the cause of this inflammation. This study aims to: (1) describe differences in the population of gut bacteria in PD compared to control subjects; (2) assess leakiness of the gut wall by differential absorption of non-absorbable sugars; (3) measure plasma levels of endotoxin and inflammation; and (4) study characteristic PD pathology and evidence of inflammation in biopsy samples of the colon obtained by sigmoidoscopy.

Study Design

Study Type
Observational
Observational Model
Case Control
Time Perspective
Cross Sectional

Eligibility Criteria

Ages
25 Years to — (Adult, Older Adult)
Sex
All
Accepts Healthy Volunteers
Yes

Inclusion Criteria

  • Not provided

Exclusion Criteria

  • Secondary or atypical parkinsonism other than Multiple System Atrophy
  • Occupation or medical treatment known to influence intestinal flora
  • Organic gastrointestinal disease other than hiatal hernia or hemorrhoids; history of gastrointestinal surgery other than remote appendectomy or cholecystectomy.
  • Acute or chronic medical illness that would confound study results.
  • Coagulopathy or use of anticoagulant medications (including aspirin).
  • Chronic use of diuretics

Outcomes

Primary Outcomes

Total urine sugar per 24 hours

Time Frame: 24 hours

Subjects consume a mixture of sugars (lactulose, sucrose), then collect urine for 24 hours. Sugar concentrations in the urine are assayed by gas chromatography.

LH-PCR fingerprint analysis

Time Frame: 24 hours

Total genomic DNA will be extracted from colonic mucosa biopsy specimens and lumenal samples, and will be amplified by PCR using bacterial primers. PCR products will be separated and analyzed for amplicon length heterogeneity.

Blood endotoxin and cytokine levels

Time Frame: 24 hours

Blood endotoxin and cytokine levels

Histopathology and immunohistochemistry of colonic mucosa

Time Frame: 24 hours

A portion of the colonic tissue will be studied with histopathology and immunohistochemistry techniques for alpha-synuclein pathology, cytokines and inflammatory markers.

Secondary Outcomes

No secondary outcomes reported

Investigators

Sponsor Class
Other
Responsible Party
Principal Investigator
Principal Investigator

Kathleen M. Shannon

Professor, Neurological Sciences

Rush University Medical Center

Study Sites (1)

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