Parkinson’s “Breakthroughs”

iStock_000009472190_DNA“Have they figured out what causes Parkinson’s?”  I got asked that question yet again the other day.  The answer (as with most Parki questions) is “sort of”.  My inability to clearly explain this answer made me vow to bone up on current science in the PD research newsfeed I get.

I have to admit I gave up looking very closely at this newsfeed (Science Daily) because every headline reads something like: “Scientists close to breakkthrough”, “Scientists discover potential cure”, “Scientists find a possible fountain of youth”.  Initially you think a cure must be right around the corner, but then you start noticing those weasel words …..and how every article ends with “More research is needed”.

It is also worth noting that much of the science journalism in this newsfeed are  press releases from a university communications department, whose mission is to present their institution on the cutting edge of research.  Who wants to read that scientists will be slogging through this experiment for the next 10 years and don’t have a clue what the results mean?  No, any red-blooded alumnus wants to read that the alma mater’s scientists are “close to a breakthrough”.

This all sounds very cynical, but my commentary is just to give a reality check on the enthusiastic headlines.  In truth the amount and diversity of Parkinson’s research is highly encouraging.  Here is a brief glimpse of research just in the last few months (all from Science Daily, follow the links to the full article).

Headline: Parkinson’s Disease biomarker found in patient urine samples (7/5/16)

Significance:  Any research that identifies biomarkers for PD is a big,big deal.   Biomarkers are the equivalent of white blood cell counts to indicate infection.  Because you can’t take (say) blood samples from the brain, biomarkers for PD are problematic.  In this case, a protein(LRRK2) found in the neurons of PD patients  was also found in urine and spinal fluid.

The catch:  LRRK2 mutations are only found in patients with hereditary PD – about 2-3% of the PD population, per this article.  But this biomarker provides a way to test the efficacy of PD drugs.  Also, in an expanded study, approximately 20 percent of people without LRRK2 mutations but with Parkinson’s disease also showed similar results.

bad_boy_2Headline:  Key to Parkinson’s disease neurodegeneration found (6/8/16)

Significance:  PD researchers have known for several years that people whose cells make too much alpha-synuclein or make a mutated form of the protein are at high risk of developing PD because of the protein’s toxicity.  What’s new in this study is why too much of this bad-boy protein is toxic: it disrupts the normal functioning of mitochondria–the tiny powerhouses responsible for generating a cell’s energy.  By attaching to a mitochondrial protein called TOM20, alpha-synuclein prevents the mitochondria from functioning optimally, which results in the production of less energy and more damaging cellular waste.

The catch:  “More research is needed” to determine if gene therapy would work to keep alpha-synuclein from sticking to TOM20.

HeadlineNew gene shown to cause Parkinson’s disease (6/6/16)

Significance:  About 15 percent of Parkinson’s disease cases are thought to be caused by genetics, primarily by mutations in two genes called SNCA and LRRK2.  (Note the 15% contrasted with 2-3% in the 7/5/16 article excerpted above.)  This study identified another gene (TMEM230) whose mutations can lead to PD.  The researchers hypothesize that TMEM230’s normal function involves release by synaptic vesicles of dopamine into different parts of the brain — and the gene’s mutations interfere with this function.

The catch:  This research so far has taken 20 years, but it’s not over yet. ” In future research, [researchers] plan to explore how TMEM230 mutations cause disease using mouse models.”

man-drinking-milkHeadline:  Pesticide found in milk decades ago may be associated with signs of Parkinson’s (12/9/15)

Significance:  The headline could easily be shortened to “Drinking milk causes Parkinson’s”, but of course the findings are more nuanced!  The study measured (in autopsy) in 116 brains the amount of residue of a pesticide called heptachlor epoxide.   The pesticide was found at very high levels in the milk supply in the early 1980s in Hawaii, where the study took place.  “The study found that nonsmokers who drank more than two cups of milk per day had 40 percent fewer brain cells in that area of the brain than people who drank less than two cups of milk per day.  For those who were smokers at any point, there was no association between milk intake and loss of brain cells.  Previous studies have shown that people who smoke have a lower risk of developing Parkinson’s disease.”  (So….drinking milk is bad and smoking is good…??)

The catch:  “Residues of heptachlor epoxide were found in 90 percent of people who drank the most milk, compared to 63 percent of those who did not drink any milk.  [The study’s author] noted that the researchers do not have evidence that the milk participants drank contained heptachlor epoxide. He also stated that the study does not show that the pesticide or milk intake cause Parkinson’s disease; it only shows an association.”  Understanding the difference between association and causation is essential for reading science journalism!

About Laura Kennedy Gould

Author of "The Magic Trick -- Life with Parkinson's
This entry was posted in Parkinson's Causes, Parkinson's Research and tagged , , , , . Bookmark the permalink.

3 Responses to Parkinson’s “Breakthroughs”

  1. John Lothian says:

    Great article! You hit the nail square on the head.

  2. Lucy Kennedy says:

    I’m so impressed with your knowledge!

  3. Thanks for these clearly written updates. It’s always good to remind ourselves that “association” does not mean “causation,” and that practically every research report concludes with “more research is needed.”

    I’m looking forward to attending the WPC in September where perhaps we will hear about really major breakthroughs.

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