Parkinson's Disease Tulip


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Old 08-25-2009, 09:19 AM #1
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Default More about wheat - getting interesting

At least to me

Let me see if I can keep this straight-
1-There is an enzyme in the gut called "tissue transglutamase", forever after known as TG2.
2- This is different than the gliadin normally blamed for celiac problems.
3- PWP tend to have antibodies to TC2. Among other things this results in inflammation.
4- TC2 is used in food processing to "glue" together the bits that would otherwise be thrown away.

From Wikipedia-
Antibodies to tissue transglutaminase are found in coeliac disease and may play a role in the small bowel damage in response to dietary gliadin that characterises this condition.

Recent research indicates that sufferers from neurological diseases like Huntington's,[5] and Parkinson's[6] may have unusually high levels of one type of transglutaminase, tissue transglutaminase. It is hypothesized that tissue transglutaminase may be involved in the formation of the protein aggregates that causes Huntington's disease, although it is most likely not required.[7]

Industrial applications
Industrial transglutaminase is produced by Streptoverticillium mobaraense fermentation in commercial quantities and is used in a variety of processes, including the production of processed meat and fish products. It can be used as a binding agent to improve the texture of protein-rich foods such as surimi or ham.

Transglutaminase can be used in these applications:

Binding small chunks of meats into a big one ("portion control"), such as in sausages, hot dogs, restructured steaks
Improving the texture of low-grade meat such as so-called "PSE meat" (pale, soft, and exudative meat; caused by stress and a rapid postmortem pH decline)
Making milk and yogurt creamier
Making noodles firmer
Besides its "orthodox" uses, transglutaminase can be used to create some unusual foods. "Cold Set Bound Fish Kebabs" are made from alternating layers of salmon and cod which are "glued" together by transglutaminase. Wylie Dufresne, chef of New York's avant-garde restaurant WD-50, invented a "pasta" made by over 95% shrimps thanks to transglutaminase.
Source(s):
http://en.wikipedia.org/wiki/Transglutam…
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
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Old 08-25-2009, 09:22 AM #2
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Default And...

1: Neurology. 2006 Feb 14;66(3):373-7.

Autoantibody targeting of brain and intestinal transglutaminase in gluten ataxia.

Hadjivassiliou M, Mäki M, Sanders DS, Williamson CA, Grünewald RA, Woodroofe NM,
Korponay-Szabó IR.

Department of Neurology, Royal Hallamshire Hospital, Sheffield, UK.
m.hadjivassiliou@sheffield.ac.uk

OBJECTIVE: To investigate the presence of autoantibody deposition against type 2
tissue transglutaminase (TG2; a reliable marker of the whole spectrum of gluten
sensitivity) in the jejunal tissue and brain of patients with gluten ataxia and
in control subjects. METHODS: The authors evaluated jejunal biopsy samples from
nine patients with gluten ataxia and seven patients with other causes of ataxia
for the presence of TG2-related immunoglobulin deposits using double-color
immunofluorescence. Autopsy brain tissue from one patient with gluten ataxia and
one neurologically intact brain were also studied. RESULTS: IgA deposition on
jejunal TG2 was found in the jejunal tissue of all patients with gluten ataxia
and in none of the controls. The intestinal IgA deposition pattern was similar to
that seen in patients with overt and latent celiac disease and in those with
dermatitis herpetiformis. Widespread IgA deposition around vessels was found in
the brain of the patient with gluten ataxia but not the control brain. The
deposition was most pronounced in the cerebellum, pons, and medulla. CONCLUSIONS:
Anti-tissue transglutaminase IgA antibodies are present in the gut and brain of
patients with gluten ataxia with or without an enteropathy in a similar fashion
to patients with celiac disease, latent celiac disease, and dermatitis
herpetiformis but not in ataxia control subjects. This finding strengthens the
contention that gluten ataxia is immune mediated and belongs to the same spectrum
of gluten sensitivity as celiac disease and dermatitis herpetiformis.


PMID: 16476935 [PubMed - indexed for MEDLINE]
__________________
Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
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