[reverett123]

As most have noticed, I am convinced that stress and inflammation interact to produce PD. This from this morning's Science Daily News adds to the picture-

".... researchers from the University of Connecticut Health Center have found that the same part of our nervous system that is responsible for the fight-or-flight response (called the sympathetic nervous system) also controls regulatory T cells, which are used by the body to end an immune response once a foreign invader has been removed or destroyed."

Here, in a nutshell, we have it.
1- The "f-o-f" response is triggered by stress
2- This affects the sympathetic nervous system which leads to poor control of T-cells
3- T cells thus become unable to end the response of the microglia in the inflammatory brain. Result is dead neurons and a sea of cytokines

It isn't an autoimmune situation where the immune system attacks our own tissues. It is a loss of the shutdown power of the T cells that are supposed to be under the control of the same part of the nervous system which responds to stress. The endocrine system pumps out cortisol in response to two things here (there are others). One, it pumps it out in response to chronic stress, the type we can't escape. Two, it pumps it out in response to inflammation, the original steroid treatment.

This would lead one to expect that cortisol levels in PWP would reflect all this.


1. Acta Neurol Scand. 1998 Feb;97(2):77-85.

Cortisol is higher in parkinsonism and associated with gait deficit.

Charlett A, Dobbs RJ, Purkiss AG, Wright DJ, Peterson DW, Weller C, Dobbs SM.

Statistics Unit, Public Health Laboratories Service, London, UK.

INTRODUCTION: We propose an active pathogenic mechanism, involving circulating
cortisol, in parkinsonism. MATERIALS AND METHODS: Serum cortisol was measured in
96 subjects with idiopathic parkinsonism, 170 without, and in 17 spouses and 36
siblings of elderly sufferers with double the number of controls, all obeying
inclusion/exclusion criteria. RESULTS: Cortisol, adjusted for sampling time, was
greater (17%, on average, P<0.001) in parkinsonians, but not in relatives. The
central cortisol lowering effect of anti-muscarinics was seen (P=0.025).
Selegiline may attenuate the disease, and parkinsonism is less frequent in
tobacco smokers. Selegiline was associated with a lower cortisol (P=0.03):
chronic smoking appeared (P=0.08) to be, irrespective of parkinsonism. Bowel
stasis has been implicated in the pathogenesis: cortisol was higher in
parkinsonians requiring laxatives (P=0.05). In controls, cortisol was lower, the
longer the stride (P=0.02): in parkinsonians, this relationship was numerically
reversed. A similar (P=0.01) group performance interaction was seen for
deterioration, over 4 years, in gait. CONCLUSION: Cortisol is doing harm or
mirroring something which is. A common pathway for neuronal protection/rescue
emerges.

PMID: 9517856 [PubMed - indexed for MEDLINE]