I was really struck by this post made by Carey; it parallels some ideas being tossed around on the PD Online Research site. Sorry, I'm too new here to post links, but if you Google the title and the author's name "Weiner", you'll get right to it. I apologize that some of you may have already discussed this, but I wanted to repost for those of us who are noobs.

Author: Weiner, William J.
Title: "There is no Parkinson Disease"
Journal: Archives of Neurology 2008 65(6)705-708

A few key excerpts from the article:

The difficulty of an accurate clinical diagnosis of Parkinson disease was highlighted by Hughes et al. Their study reported the pathologic findings in 100 consecutive patients clinically diagnosed as having Parkinson disease (the mean age at symptom onset was 64.5 years, and the mean disease duration at autopsy was 11.9 years). Of 100 patients diagnosed as having Parkinson disease, 76 had pathologic confirmation. The "misdiagnosed" cases included progressive supranuclear palsy, multiple system atrophy, Alzheimer disease, vascular nigral atrophy, postencephalitis, and healthy brain. This study illustrates the problems in clinical diagnosis. Of the patients misdiagnosed as having Parkinson disease, 67% had a marked initial response to levodopa treatment (>50% improvement). So much for levodopa responsiveness as a clinical criterion for the diagnosis of "true" Parkinson disease. Hughes et al, commenting on whether Parkinson disease is a clinically diagnosable specific entity, wrote, "Until biological markers or other techniques are developed, we must accept that diverse neuropathologic disorders may produce clinical syndromes indistinguishable from Lewy Body Parkinson's disease."

Furthermore..."Is it possible that recent neuroprotective trials for Parkinson disease have failed because numerous subtypes of Parkinson disease are lumped together? We know little about how these abnormal genes, their end products, or their mechanisms of action regarding cell degeneration and cell death operate. However, each of the abnormal genes identified thus far is speculatively linked to different biological mechanisms (eg, LRRK2 kinase activity and the parkin-ubiquitin-proteasome system)"


As someone who does not have what is now being studied as a possible major biomarker like diminished sense of smell, I wonder how many people might be further misdiagnosed or missed diagnosed if we don't start linking these broad based research avenues to genetic information that we do have?

I'm sure that the above article is not news, but I think it deserves to be a basis for redefining the whole PD research culture and standard clinical control measurements (over-reliance on placebo that by it's very nature is highly dubious because of its direct correlation to dopamine).