This thread appears to be based on a paper by Fitzmaurice et al. [1]. Unfortunately this is behind a pay wall. The paper's abstract, however, is available. In it the authors propose:
"that benomyl, via its bioactivated thiocarbamate sulfoxide metabolite, inhibits aldehyde dehydrogenase (ALDH), leading to accumulation of the reactive dopamine metabolite 3,4-dihydroxyphenylacetaldehyde (DOPAL), preferential degeneration of dopaminergic neurons, and development of PD."

So, the claim, as I understand it, is that, at least in part, PD is caused by the inhibition of ALDH.

This suggests to me that further work is needed to see whether this could lead to possible therapies based on alcohol and tea.

Chrostek et al. write [2]:
"Chronic ethanol consumption significantly increased the liver ALDH activity in young and adult rats but decreased this activity in old animals. The drinking of green tea did not alter ALDH activity in ethanol-consuming rats. Drinking green tea alone significantly increased ALDH activity in young and adult rats but did not alter this activity in old rats."

I can't find a clear picture of the relationship between PD and alcohol, but a feature article in Neurology Review [3] says:
"People who moderately consume beer may reduce their risk of developing Parkinson’s disease by 27%, compared with nondrinkers."

The picture with green tea is also unclear, but Quintana [4] states:
"There was a clear protective effect of tea consumption in the pooled risk estimate [OR: 0.83 (95% confidence interval 0.74 to 0.92)] with 2215 cases and 145578 controls."

In writing this post I came across a thread [5] from two years ago started by cockankat, to whom my thanks, that reports on the relationship between ALDH and DOPAL and reports that
"analysis of 14 brains of people who died with Parkinson disease had 4.4 times more DOPAL than the brains of people without Parkinson disease" and that ALDH is deficient in PwP.

References

[1] "Aldehyde dehydrogenase inhibition as a pathogenic mechanism in Parkinson disease"
Arthur G. Fitzmaurice, Shannon L. Rhodes, Aaron Lulla, Niall P. Murphy, Hoa A. Lam, Kelley C. O’Donnell, Lisa Barnhill, John E. Casida, Myles Cockburn, Alvaro Sagasti, Mark C. Stahl, Nigel T. Maidment, Beate Ritz, Jeff M. Bronstein
PNAS, vol 110, no 2.
http://www.pnas.org/content/110/2/636.abstract

[2] "The effect of green tea on the activity of aldehyde dehydrogenase (ALDH) in the liver of rats during chronic ethanol consumption."
Chrostek L, Tomaszewski W, Szmitkowski M.
Rocz Akad Med Bialymst. 2005;50:220-3.
http://www.ncbi.nlm.nih.gov/pubmed/16358971

[3] "Does Alcohol Consumption Reduce the Risk of Parkinson’s Disease?"
Neurology Reviews
2011;19(12)14-15.
http://www.neurologyreviews.com/Arti...SI=&FullText=1

[4] "Parkinson's Disease and Tea: A Quantitative Review"
José Luis Barranco Quintana, MD, MPH,
Mohamed Farouk Allam, MPH, PhD,
Amparo Serrano Del Castillo, MD, PhD and
Rafael Fernández-Crehuet Navajas, MD, PhD
J Am Coll Nutr February 2009 vol. 28 no. 1 1-6
http://www.jacn.org/content/28/1/1.full

[5] http://neurotalk.psychcentral.com/sh...highlight=aldh

John