Lipopolysaccharide Animal Models for Parkinson's Disease
 

Is lipopolysaccharide (LPS), an endotoxin from bacterial cell walls, merely a research tool to investigate microglial activation and neuronal damage or a real world cause of PD?

http://www.hindawi.com/journals/pd/2011/327089/

"LPS acts as an endotoxin and elicits multiple pathological effects in human beings. One case report may uncover a potential link between LPS infection and the development of Parkinsonism. A 22-year-old laboratory worker was accidentally exposed to 10 μg Salmonella minnesota LPS through an open wound and developed Parkinson’s syndrome with bradykinesia, rigidity, tremor, and cogwheel phenomenon three weeks later; damage to the substantia nigra and cerebral cortex was shown by positron emission tomography a few years after the accident."

Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration
 

More evidence that systemic LPS may affect the brain.

http://www.ncbi.nlm.nih.gov/pubmed/17203472

"Systemic LPS administration resulted in rapid brain TNFalpha increase that remained elevated for 10 months, while peripheral TNFalpha (serum and liver) had subsided by 9 h (serum) and 1 week (liver). Systemic TNFalpha and LPS administration activated microglia and increased expression of brain pro-inflammatory factors (i.e., TNFalpha, MCP-1, IL-1beta, and NF-kappaB p65) in wild-type mice, but not in TNF R1/R2(-/-) mice. Further, LPS reduced the number of tyrosine hydroxylase-immunoreactive neurons in the substantia nigra (SN) by 23% at 7-months post-treatment, which progressed to 47% at 10 months. "