New research examines connection between inflammatory stimulus and Parkinson's disease

Public release date: 23-Apr-2013 [ | E-mail | Share ]

Contact: Donna Krupa dkrupa@the-aps.org 617-954-3976 Federation of American Societies for Experimental Biology

BOSTONParkinson's disease (PD) is a progressive degenerative disease affecting a person's ability to coordinate and control their muscle movement. What starts out as a tremor in a finger will eventually lead to difficulty in writing and speaking, and ultimately the inability to walk without assistance. Since the 1950s research has shown that people with Parkinson's have decreased levels of the chemical dopamine in their brains, which is involved in sending messages to the part of the brain that controls coordination and movement. Subsequent research has found that dopamine-generating cells, known as dopaminergic neurons, are also absent in a specific area of the brain in those with PD.

The precise cause or causes of PD is unknown, but there is a consensus that an inflammatory event or episode is involved in the initiation of neurodegeneration, and that chronic neuroinflammation is a sustaining and exacerbating reason for the loss of the dopaminergic neurons. A new study conducted by a team of Texas researchers brings the understanding of inflammation's role a step further. They have found that a single, high-dose exposure of an experimental inflammatory agent in an animal model causes changes in brain tissue that are similar to those associated with the development of the disease.

The study was conducted by Roger Bick and his colleagues Marie-Francoise Doursout, Michael S. Schurdell, Lauren M. Young, Uzondu Osuagwu, Diana M. Hook, Brian J. Poindexter, Mya C. Schiess, and Diane L. M. Bick, all at the University of Texas Health Science Center, Houston, Tex. Dr. Schiess will discuss the team's findings at the Experimental Biology 2013 meeting, being held April 20-24, 2013 at the Boston Convention and Exhibition Center, Boston, Mass.

The poster presentation is entitled, "Inflammatory cells and cytokines in the olfactory bulb of a rat model of neuroinflammation; Insights into neurodegeneration?" and is sponsored by the American Society for Investigative Pathology (ASIP), a co-sponsor of the meeting. The full study will appear this month in the online edition of the Journal of Interferon & Cytokine Research.

Methodology

In the study, the researchers examined inflammatory cell and cytokine production in brain tissue from a lipopolysaccharide (LPS)-treated rat model that mimics many of the neuropathologic changes associated with PD. Concurrently, they monitored the appearance of glial cell line-derived neurotrophic factor (GDNF), a neuronal protective agent, and circulating nitric oxide (NO) levels. They also examined the immune system associated cells in the olfactory bulb of the brain. It is known that Parkinson's starts with this mechanism.

Twelve male Sprague-Dawley rats were treated with intravenous LPS in saline, 12 control rats were treated with saline, and all were maintained for up to 48 hours before euthanasia and brain removal. Brains were removed from both groups at defined times, blood and other tests were conducted, and images of various sections of the brain, including the olfactory bulb, cortex and cerebellum, were taken using fluorescent microscopy.

Results and Conclusions

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New research examines connection between inflammatory stimulus and Parkinson's disease