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Wake up and smell the … curry?

Posted by on May 24, 2013

Professor Roger Bick MMedEd MBS is a researcher in the department of Pathology and Laboratory Medicine at the University of Texas.

Every time I walk past an Indian restaurant my nasal passages expand, my salivary glands produce more saliva and I look to see if I have enough time to scarf down some tandoori chicken. I can’t image not enjoying that enticing smell; or the smell of cut grass; or of leather. Yet the loss of olfaction, the ability to smell, is just one of the early symptoms of Parkinson’s that so many have to suffer.

Parkinson’s (PD) is a devastating disease that often affects a person for many years, and is associated with a multitude of problems. There is a system, the Hoehn and Yahr system, which lists five stages through which patients experience.

Individuals progress from ‘inconvenient’ symptoms, through the onset of gait and posture problems, to the inability to stand or walk. This leads to a complete loss of independence, meaning the patient requires home assistance and constant care. One symptom, an early indicator of impending trouble, is the loss of the ability to smell.

Alongside a team of researchers at the University of Texas Medical School, we studied the hypothesis that inflammation initiates changes within the brain and so could be linked to the onset of PD. To test this hypothesis, we researched inflammation in rat brains and used microscopic imaging of the olfactory bulb, an organ that sends smell signals from your nose to your brain.

We tested the idea that when smell signals are sent to the brain, the resulting inflammation causes immune cell invasion, leading to the increased influx of small signalling molecules such as cytokines and nitric oxide. The influx of these molecules activates glial cells, the ‘scavenger cells’ of the brain, leading to an increased production of a protective substance, glial cell line-derived neurotrophic factor.

So, when we measured how many immune cells were in the olfactory bulb after initiating inflammation, we saw a tremendous increase in some and then a rapid decrease. Meanwhile, lymphocyte (white blood cells) numbers remained high for a long while, often gathering around blood vessels.

This suggests that the wellbeing of the blood brain barrier and immune cells have a significant role in nerve cell destruction leading to PD.

Neuroinflammation is an early problem with PD and it persists throughout the course of this debilitating illness, while molecules made by specific cells have been implicated in giving at least some protection to dopaminergic nerve cells. However, cells outside the central nervous system do appear to have a role in the initiation and continuation of PD’s pathology.

Our studies support such a line of thought in which balances in pro-inflammatory molecules and the production of protective enzymes exist in a finely tuned balance, a balance that is chaotically altered in response to a severe inflammation and possibly subsequent inflammatory episode(s) that kill previously injured neurons. This balance remains a target for therapeutic challenges.


The work was presented at:-

And the research was carried out in the departments of Pathology, Anesthesiology and Neurology at the University of Texas Medical School at Houston by Roger J. Bick, PhD, MMEd, MSB, FAHA; Marie-Francois Doursout, PhD; Diane L. M. Bick, PhD, FAHA; Mya C. Schiess, MD; Diane Hook-Dufresne, MD; Brain J. Poindexter, MS; Uzondu Osuagwu, MD; Lauren Young-Lobaugh, MD and Michael Schurdell, MD. The authors gratefully acknowledge the assistance of Donna Krupa, Director of Communications, American Physiological Society, in the publication and preparations of articles associated with this work.



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