[olsen]

Rick--interesting comments in light of your theory that PD may be caused by a "prenatal event" to be activated/triggered later in life:

http://www.nature.com/bjp/journal/va.../0707167a.html

British Journal of Pharmacology advance online publication 5 March 2007; doi: 10.1038/sj.bjp.0707167

Inflammation as a causative factor in the aetiology of Parkinson's disease

P S Whitton1



conclusion from above linked article:

"PD is a relatively common neurodegenerative disease with a well-characterized group of symptoms. Although a number of different mechanisms have been proposed in the aetiology of PD, none have been considered to have absolute predominance. In part, this has been due to the difficulty in establishing any clear epidemiology for idiopathic PD, which is responsible for some 95% of cases. Indeed, on the face of it, idiopathic PD appears to strike at random with no apparent pattern either geographically or among patient groups. The observations in patients and experimental models of PD that neuroinflammation appears to be one of the, if not the, most consistant pathological change, opens new possibilities in understanding this illness. The CNS had been considered to be a relatively immunologically quiescent organ but this is now undergoing a considerable re-evaluation. It has become apparent from a number of lines of research, including a substantial volume relating to PD, that microglial cells can become activated by a wide range of stimuli. Critically, these include infections of peripheral origin. The findings by Ling et al. (2002, 2006) that prenatal infection of female rats leads to progressive neuroinflammatory and degenerative PD-like changes in the offspring, following a subsequent LPS challenge, are of great interest. The implication is that a predisposition to SN neurodegeneration may be established before birth or possibly by infections afterwards. That these could in part underlie a disease that might not emerge until decades later could indeed account for the difficulty in 'predicting' PD, as the events would be highly unlikely to be connected. The potential use of anti-inflammatory drugs in PD is interesting but it is hard to envisage great benefit unless the intervention is made with a very early diagnosis leading to the possibility that calming the neuroinflammatory crisis in the SN might at least slow disease progression."

(I include only the 2 references the author cites in this conclusion-- the rest are obtainable from the article

Ling Z, Gayle DA, Ma SY, Lipton JW, Tong CW, Hong JS (2002). In utero bacterial endotoxin exposure causes loss of tyrosine hydroxylase neurons in the postnatal rat midbrain. Movement Dis 17: 116–124. | PubMed |

Ling Z, Zhu Y, Tong CW, Snyder JA, Lipoton JW, Carvey PM (2006). Progressive dopamine neuron loss following supra-nigral lipopolysaccharide (LPS) infusion into rats exposed to LPS prenatally. Exp Neurol 199: 499–512. | Article | PubMed | ChemPort |


(there's that smiley face again--I could not even edit it out! Madelyn)