Heidi - do you suggest that researchers cannot see the forest?

Something like that.

I just know there's a lot of time, money and energy being spent on the minutest biochemical pathways. And the most elegant experiment I've seen in a long time is the antigliadin binding study referenced in my paper. He just took some antibodies, poured them on some brain tissue and analyzed what happened. Brilliant.
I wrote to him and asked him to do it in every combination possible. Gluten antibodies on pancreas. Casein antibodies on brain. Etc.

I have the full article if anyone wants it.

Hello, Heidi, I wish I had time to read this entire thread now. I'm wondering if your theory fits in with new research regarding LRRK2 mutations:

http://hmg.oxfordjournals.org/cgi/content/full/16/2/223

Parkinson's disease-associated mutations in LRRK2 link enhanced GTP-binding and kinase activities to neuronal toxicity

Human Molecular Genetics Advance Access originally published online on January 2, 2007

Thanks.

By the way, I have bad allergies and have lived on antihistamines since I was a kid. So did my dad, who had PD. I also had some autoimmune problems in the 80's with discoid lupus, confirmed by biopsy.

ZF-
I'm kind of getting out of my range here, but let me tell you how I imagine the process:

The binding of antigliadin to Synapsin I prevents neurotransmitter release (exocytosis). The process of exocytosis has been shown to be the trigger which facilitates the dispersion of excess alpha-synuclein from the cell body. If exocytosis is interrupted, excess alpha-synuclein remains in the nerve terminal.
The fibril form of alpha-synuclein is stiff and pointy and pokes holes in the cellular membranes like the nucleus, mitochondria and golgi complex. To protect itself the cell folds it up and covers it with other proteins creating Lewy Bodies. Parkin and ubiquitin are two of the proteins involved in that process. People with parkin mutation don't make Lewy bodies and their cells die faster. It looks like LRRK2 is also one of those "waste processing" proteins, it binds to parkin, and is found in Lewy bodies in the few studies that have been done. LRRK2 mutations result in rapid cell degeneration.

If that sequence is correct, then the goal is the same but more time-critical: to avoid the excess alpha-synuclein in the first place.

I've got a bunch of abstracts in a couple docs here, not very tidy, but I'll send them to you if you want.

-H

ps. Cara has links to lupus articles here. Scroll about halfway down.

I know there aren't any scientific citations in this article, but I wanted to follow up to this.
As a young researcher, I believe that the old "permeable/nonpermeable" BBB theory is wrong. To believe that the brain should be somehow immunologically privileged is incorrect, in my opinion. Besides that, even if it should, we ALL have so many low-level (and sometimes not so low-level) chronic viral infections (herpes simplex, and epstein barr are the most notable) and chronic bacterial infections (queue Streptococcus), that, in theory, our brains are open playing fields for immune effector molecules.

There is an article illustrating that antibodies go in and play with the brain some, but I will try and come back to post it later (no link capabilities yet). Search Huffington post, and gluten impacts the brain.


Celiac disease runs very strong on both sides of my family - yet I am the only one who follows GF. My grandfather (and all of his siblings) has a mild from of early-onset Parkinsons - it kills me to think that GF many years ago could have saved his brain.

I'm not sure-wanted to check- by GF do you mean gluten free?
or Genome Factor? Growth Factor? Thanks!

By coincidence I ran up against Mr. Wheat again today when I had an early lunch and could not resist the restaurant's fried chicken. I barely made it home.

Because I have been doing well with the perindopril and have been successfully avoiding gluten as well, the contrast was startling. Within an hour I was unable to walk and was non-responsive to meds. It has been six hours and I am only now getting back to normal.

A couple of hypotheses- Maybe the BBB was, indeed, temporarily breached as the result of an inflammatory response. Or perhaps there was enough rise in my blood pressure to create a similar effect. Or, most likely, a combination of both.

In any case, there were both physical and cognitive effects.