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

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.

Inclusion criteria

--Parkinson's disease:

• Clinically diagnosed Parkinson's disease
• Hoehn & Yahr stage 1-2.5
• No symptomatic treatment of Parkinson's disease symptoms

Inclusion criteria

--Multiple System Atrophy

• Clinically diagnosed Multiple System Atrophy.

Inclusion criteria

--Control subjects:

• No diagnosis of Parkinson's disease and no signs of Parkinson's disease on screening neurological examination

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