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home:diseases:parkinsons [01.10.2019] – [Gastrointestinal inflammation] sallieqhome:diseases:parkinsons [09.14.2022] (current) – external edit 127.0.0.1
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 ====== Parkinson's disease ====== ====== Parkinson's disease ======
  
-[[http://www.mayoclinic.org/diseases-conditions/parkinsons-disease/basics/definition/con-20028488|Mayo Clinic overview]]+[[https://www.mayoclinic.org/diseases-conditions/parkinsons-disease/basics/definition/con-20028488|Mayo Clinic overview]]
  
  
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 RESULTS: The probabilities of random occurrence (P values) in the 3 clusters were P = 7.9 x 10 (-7)for cluster 1, P = 2.6 x 10 (-7)for cluster 2, and P = 1.5 x 10 (-7)for cluster 3.  RESULTS: The probabilities of random occurrence (P values) in the 3 clusters were P = 7.9 x 10 (-7)for cluster 1, P = 2.6 x 10 (-7)for cluster 2, and P = 1.5 x 10 (-7)for cluster 3. 
  
-CONCLUSIONS: Our findings indicate an important role for environmental causation in Parkinson disease. A possible role exists for environmental factors such as viral infection and toxins in the light of current evidence.  (({{pubmed>long:15262735}}))+CONCLUSIONS: Our findings indicate an important role for environmental causation in Parkinson disease. A possible role exists for environmental factors such as viral infection and toxins in the light of current evidence.  (({{pmid>long:15262735}}))
  
 ===== Gastrointestinal inflammation ===== ===== Gastrointestinal inflammation =====
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 <blockquote> <blockquote>
  
-Colonoscopy or flexible sigmoidoscopy may be used to predict Parkinson's  (({{pubmed>long:22550057}})) (({{pubmed>long:26539989}})) (({{pubmed>long:26179554}}))+Colonoscopy or flexible sigmoidoscopy may be used to predict Parkinson's  (({{pmid>long:22550057}})) (({{pmid>long:26539989}})) (({{pmid>long:26179554}}))
  
 </blockquote> </blockquote>
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 <blockquote>OBJECTIVE:An inflammation-driven model of PD has been proposed based on the endotoxin lipopolysaccaride (LPS), a potential source of inflammation in the gastrointestinal system linked to neurotoxicity. Systemic exposure to bacterial endotoxin (LPS) can be determined by measuring plasma LPS binding protein (LBP). We aimed to evaluate whether lipopolysaccharide binding protein (LBP) can be used to distinguish PD subjects from control subjects and to assess whether LBP levels correlate with PD disease severity. <blockquote>OBJECTIVE:An inflammation-driven model of PD has been proposed based on the endotoxin lipopolysaccaride (LPS), a potential source of inflammation in the gastrointestinal system linked to neurotoxicity. Systemic exposure to bacterial endotoxin (LPS) can be determined by measuring plasma LPS binding protein (LBP). We aimed to evaluate whether lipopolysaccharide binding protein (LBP) can be used to distinguish PD subjects from control subjects and to assess whether LBP levels correlate with PD disease severity.
  
-CONCLUSIONS: Our data suggests that LBP is one GI biomarker related to LPS induced neurotoxicity. However, there was significant variability in LBP levels within the PD and control groups, limiting its utility as a stand-alone biomarker.  //Pal et al// Front Neurosci. 2015 Sep 1 (({{pubmed>long:26388718}}))</blockquote> +CONCLUSIONS: Our data suggests that LBP is one GI biomarker related to LPS induced neurotoxicity. However, there was significant variability in LBP levels within the PD and control groups, limiting its utility as a stand-alone biomarker.  //Pal et al// Front Neurosci. 2015 Sep 1 (({{pmid>long:26388718}}))</blockquote> 
  
 <blockquote>Strong epidemiologic evidence suggests that smokers and coffee drinkers have a lower risk of Parkinson's disease (PD). The explanation for this finding is still unknown, and the discussion has focused on two main hypotheses. <blockquote>Strong epidemiologic evidence suggests that smokers and coffee drinkers have a lower risk of Parkinson's disease (PD). The explanation for this finding is still unknown, and the discussion has focused on two main hypotheses.
  
-We propose an alternative third hypothesis, in which both cigarette and coffee consumption change the composition of the microbiota in the gut in a way that mitigates intestinal inflammation.   //Derkinderen et al//  Mov Disord. 2014 Jul 29  (({{pubmed>long:24753353}}))</blockquote>+We propose an alternative third hypothesis, in which both cigarette and coffee consumption change the composition of the microbiota in the gut in a way that mitigates intestinal inflammation.   //Derkinderen et al//  Mov Disord. 2014 Jul 29  (({{pmid>long:24753353}}))</blockquote>
  
 ===== Neuropathology ===== ===== Neuropathology =====
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 <blockquote>Helicobacter. 2005 Aug;10(4):276-87. <blockquote>Helicobacter. 2005 Aug;10(4):276-87.
 Role of chronic infection and inflammation in the gastrointestinal tract in the etiology and pathogenesis of idiopathic parkinsonism. Part 2: response of facets of clinical idiopathic parkinsonism to Helicobacter pylori eradication. A randomized, double-blind, placebo-controlled efficacy study. Role of chronic infection and inflammation in the gastrointestinal tract in the etiology and pathogenesis of idiopathic parkinsonism. Part 2: response of facets of clinical idiopathic parkinsonism to Helicobacter pylori eradication. A randomized, double-blind, placebo-controlled efficacy study.
-Bjarnason IT, Charlett A, Dobbs RJ, Dobbs SM, Ibrahim MA, Kerwin RW, Mahler RF, Oxlade NL, Peterson DW, Plant JM, Price AB, Weller C.  (({{pubmed>long:16104942}}))</blockquote>+Bjarnason IT, Charlett A, Dobbs RJ, Dobbs SM, Ibrahim MA, Kerwin RW, Mahler RF, Oxlade NL, Peterson DW, Plant JM, Price AB, Weller C.  (({{pmid>long:16104942}}))</blockquote>
  
 Section of Neuropharmacology, Institute of Psychiatry, London, UK. Section of Neuropharmacology, Institute of Psychiatry, London, UK.
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 Helicobacter. 2005 Oct;10(5):557. Bjarnason, Inguar T [corrected to Bjarnason, Ingvar T]. Helicobacter. 2005 Oct;10(5):557. Bjarnason, Inguar T [corrected to Bjarnason, Ingvar T].
 Abstract Abstract
-BACKGROUND: Links between etiology/pathogenesis of neuropsychiatric disease and infection are increasingly recognized. AIM: Proof-of-principle that infection contributes to idiopathic parkinsonism. METHODS: Randomized, double-blind, placebo-controlled efficacy study of proven Helicobacter pylori eradication on the time course of facets of parkinsonism. Intervention was 1 week's triple eradication therapy/placebos. Routine deblinding at 1 year (those still infected received open-active), with follow-up to 5 years post-eradication. Primary outcome was mean stride length at free-walking speed, sample size 56 for a difference, active vs. placebo, of 3/4 (between-subject standard deviation). Recruitment of subjects with idiopathic parkinsonism and H. pylori infection was stopped at 31, because of marked deterioration with eradication failure. Interim analysis was made in the 20 who had reached deblinding, seven of whom were receiving antiparkinsonian medication (long-t(1/2), evenly spaced) which remained unchanged. RESULTS: Improvement in stride-length, on active (n = 9) vs. placebo (11), exceeded size of effect on which the sample size was calculated when analyzed on intention-to-treat basis (p = .02), and on protocol analysis of six weekly assessments, including (p = .02) and excluding (p = .05) those on antiparkinsonian medication. Active eradication (blind or open) failed in 4/20, in whom B-lymphocyte count was lower. Their mean time course was: for stride-length, -243 (95% CI -427, -60) vs. 45 (-10, 100) mm/year in the remainder (p = .001); for the ratio, torque to extend to flex relaxed arm, 349 (146, 718) vs. 58 (27, 96)%/ year (p < .001); and for independently rated, visual-analog scale of stance-walk videos (worst-best per individual identical with 0-100 mm), -64 vs. -3 mm from anterior and -50 vs. 11 lateral (p = .004 and .02). CONCLUSIONS: Interim analysis points to a direct or surrogate (not necessarily unique) role of a particular infection in the pathogenesis of parkinsonism. With eradication failure, bolus release of antigen from killed bacteria could aggravate an effect of ongoing infection.+ 
 +BACKGROUND: Links between etiology/pathogenesis of neuropsychiatric disease and infection are increasingly recognized. AIM: Proof-of-principle that infection contributes to idiopathic parkinsonism.  
 + 
 +METHODS: Randomized, double-blind, placebo-controlled efficacy study of proven Helicobacter pylori eradication on the time course of facets of parkinsonism. Intervention was 1 week's triple eradication therapy/placebos. Routine deblinding at 1 year (those still infected received open-active), with follow-up to 5 years post-eradication. Primary outcome was mean stride length at free-walking speed, sample size 56 for a difference, active vs. placebo, of 3/4 (between-subject standard deviation). Recruitment of subjects with idiopathic parkinsonism and H. pylori infection was stopped at 31, because of marked deterioration with eradication failure. Interim analysis was made in the 20 who had reached deblinding, seven of whom were receiving antiparkinsonian medication (long-t(1/2), evenly spaced) which remained unchanged.  
 + 
 +RESULTS: Improvement in stride-length, on active (n = 9) vs. placebo (11), exceeded size of effect on which the sample size was calculated when analyzed on intention-to-treat basis (p = .02), and on protocol analysis of six weekly assessments, including (p = .02) and excluding (p = .05) those on antiparkinsonian medication. Active eradication (blind or open) failed in 4/20, in whom B-lymphocyte count was lower. Their mean time course was: for stride-length, -243 (95% CI -427, -60) vs. 45 (-10, 100) mm/year in the remainder (p = .001); for the ratio, torque to extend to flex relaxed arm, 349 (146, 718) vs. 58 (27, 96)%/ year (p < .001); and for independently rated, visual-analog scale of stance-walk videos (worst-best per individual identical with 0-100 mm), -64 vs. -3 mm from anterior and -50 vs. 11 lateral (p = .004 and .02).  
 + 
 +CONCLUSIONS: Interim analysis points to a direct or surrogate (not necessarily unique) role of a particular infection in the pathogenesis of parkinsonism. With eradication failure, bolus release of antigen from killed bacteria could aggravate an effect of ongoing infection.
  
  
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 <blockquote>   Ulcer bacteria may contribute to development of Parkinson's disease <blockquote>   Ulcer bacteria may contribute to development of Parkinson's disease
  
-http://www.eurekalert.org/pub_releases/2011-05/asfm-ubm051811.php+https://www.eurekalert.org/pub_releases/2011-05/asfm-ubm051811.php
  
 NEW ORLEANS, LA – May 22, 2011 -- The stomach bacteria responsible for ulcers could also play a role in the development of Parkinson's disease according to research presented today at the 111th General Meeting of the American Society for Microbiology. NEW ORLEANS, LA – May 22, 2011 -- The stomach bacteria responsible for ulcers could also play a role in the development of Parkinson's disease according to research presented today at the 111th General Meeting of the American Society for Microbiology.
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 Studies in the Role of chronic infection and inflammation in the gastrointestinal tract in the etiology and pathogenesis of idiopathic parkinsonism.  Dobbs RJ1, Dobbs SM, Weller C, Bjarnason IT, Oxlade NL, Charlett A  et al Studies in the Role of chronic infection and inflammation in the gastrointestinal tract in the etiology and pathogenesis of idiopathic parkinsonism.  Dobbs RJ1, Dobbs SM, Weller C, Bjarnason IT, Oxlade NL, Charlett A  et al
  
-AIM: To consider the candidature of Helicobacter in parkinsonism with cachexia. (({{pubmed>long:16104942}}))+AIM: To consider the candidature of Helicobacter in parkinsonism with cachexia. (({{pmid>long:16104942}}))
  
-AIM: Proof-of-principle that infection contributes to idiopathic parkinsonism. (({{pubmed>long:16104943}}))+AIM: Proof-of-principle that infection contributes to idiopathic parkinsonism. (({{pmid>long:16104943}}))
  
-AIM: To explore the cross-sectional fit of parkinsonism as an extra-alimentary consequence of Helicobacter pylori, using the serum antibody profile. (({{pubmed>long:16104944}}))+AIM: To explore the cross-sectional fit of parkinsonism as an extra-alimentary consequence of Helicobacter pylori, using the serum antibody profile. (({{pmid>long:16104944}}))
  
-Abstract: We challenge the concept of idiopathic parkinsonism (IP) as inevitably progressive neurodegeneration (({{pubmed>long:19250506}})) (({{pubmed>long:20633189}}))+Abstract: We challenge the concept of idiopathic parkinsonism (IP) as inevitably progressive neurodegeneration (({{pmid>long:19250506}})) (({{pmid>long:20633189}}))
  
 <blockquote>Med Hypotheses. 2010 May;74(5):895-7. Epub 2009 Dec 3. <blockquote>Med Hypotheses. 2010 May;74(5):895-7. Epub 2009 Dec 3.
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 Abstract Abstract
  
-Antibiotic therapy to eradicate Helicobacter pylori, the causative agent of gastric and duodenal ulcers, has been suggested to improve L-DOPA bioavailability in Parkinson's and thereby improve patient symptomology. To date, there has been no proven mechanism to explain the purported benefit of treatment of H. pylori in the management of Parkinson's disease. I propose the hypothesis, and provide initial data, that the mechanism of action is due to direct utilization of L-DOPA by H. pylori to maintain its ecological niche within the gastrointestinal tract. In support of this hypothesis, data is presented which demonstrates for the first time the ability of L-DOPA to influence the in vitro growth of H. pylori in an iron-restricted minimal medium. H. pylori utilization of L-DOPA for its own growth requirement reduces the amount of per orally administered L-DOPA that would be available to the patient for the treatment of Parkinson's disease-related pathology. Neuroendocrine-mediated interactions with bacteria represent the emerging interdisciplinary field of microbial endocrinology. Thus, microbial endocrinology provides for a mechanism between L-DOPA and H. pylori with which to explain the purported benefit of H. pylori-directed antibiotic therapy to improve L-DOPA bioavailability in Parkinson's patients and thereby improve drug therapy management. Further, if other bacterial species within the gastrointestinal tract depend on the availability of L-DOPA or other similar neuroendocrine-based drugs for their survival, then the efficacy of such neuroendocrine-based drugs not restricted solely for the management of parkinsonian symptomology may also be adversely affected and may therefore justify the use of an antibiotic regimen to eradicate them.  (({{pubmed>long:19962247}})) </blockquote>+Antibiotic therapy to eradicate Helicobacter pylori, the causative agent of gastric and duodenal ulcers, has been suggested to improve L-DOPA bioavailability in Parkinson's and thereby improve patient symptomology. To date, there has been no proven mechanism to explain the purported benefit of treatment of H. pylori in the management of Parkinson's disease. I propose the hypothesis, and provide initial data, that the mechanism of action is due to direct utilization of L-DOPA by H. pylori to maintain its ecological niche within the gastrointestinal tract. In support of this hypothesis, data is presented which demonstrates for the first time the ability of L-DOPA to influence the in vitro growth of H. pylori in an iron-restricted minimal medium. H. pylori utilization of L-DOPA for its own growth requirement reduces the amount of per orally administered L-DOPA that would be available to the patient for the treatment of Parkinson's disease-related pathology. Neuroendocrine-mediated interactions with bacteria represent the emerging interdisciplinary field of microbial endocrinology. Thus, microbial endocrinology provides for a mechanism between L-DOPA and H. pylori with which to explain the purported benefit of H. pylori-directed antibiotic therapy to improve L-DOPA bioavailability in Parkinson's patients and thereby improve drug therapy management. Further, if other bacterial species within the gastrointestinal tract depend on the availability of L-DOPA or other similar neuroendocrine-based drugs for their survival, then the efficacy of such neuroendocrine-based drugs not restricted solely for the management of parkinsonian symptomology may also be adversely affected and may therefore justify the use of an antibiotic regimen to eradicate them.  (({{pmid>long:19962247}})) </blockquote>
  
  
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 <blockquote>I am a Parkinson's patient and on the MP since Sept 2008. I am currently halfway phase 3. The results in summary: The progression of the disease has not stopped (maybe slowed down?). <blockquote>I am a Parkinson's patient and on the MP since Sept 2008. I am currently halfway phase 3. The results in summary: The progression of the disease has not stopped (maybe slowed down?).
  
-I know one other person on the MP who thinks he has Parkinson's. He is also in phase 3 but not reporting on an MP site. I am reporting as EpoxyJan since Oct.2009 on the study site [[http://www.marshallprotocol.com/forum35/13482.html|here]].+I know one other person on the MP who thinks he has Parkinson's. He is also in phase 3 but not reporting on an MP site. I am reporting as EpoxyJan since Oct.2009 on the study site [[https://www.marshallprotocol.com/forum35/13482.html|here]].
  
 //**EpoxyJan**, MarshallProtocol.com//</blockquote> //**EpoxyJan**, MarshallProtocol.com//</blockquote>
  
-===== Recent research and further reading =====+===== Research and further reading =====
    
-<blockquote>Towards this end, we used a published dataset to analyse bacteriophage composition and determine the phage/bacteria ratio in faecal samples from drug-naive PD patients and healthy participants. Our analyses revealed significant alterations in the representation of certain bacteriophages in the phagobiota of PD patients. (({{pubmed>long:30018338}})) </blockquote>+<blockquote>Towards this end, we used a published dataset to analyse bacteriophage composition and determine the phage/bacteria ratio in faecal samples from drug-naive PD patients and healthy participants. Our analyses revealed significant alterations in the representation of certain bacteriophages in the phagobiota of PD patients. (({{pmid>long:30018338}})) </blockquote>
  
-[[http://books.google.com/books?id=REICWr22YR8C&dq=Parkinson's:+another+look.+Is+Parkinson's+disease+caused+by+a+bacteria%3F&printsec=frontcover&source=bn&hl=en&ei=Khj-SZmdFaCltgegm62SDA&sa=X&oi=book_result&ct=result&resnum=4|Parkinson's Another Look]]+<blockquote>In 1919, it was first recognized that loss of pigmentation in the substantia nigra of the midbrain is a feature   (({{pmid>long:29261972}}))   </blockquote> 
 + 
 +The implication of tyrosine hydroxylase (TH), the enzyme that catalyzes the formation of L-3,4-dihydroxyphenylalanine, in the pathogenesis of PD at different levels makes it a promising candidate for developing efficient treatment based on correcting or bypassing the enzyme deficiency. (({{pmid>long:22483311}})) 
 + 
 +[[https://books.google.com/books?id=REICWr22YR8C&dq=Parkinson's:+another+look.+Is+Parkinson's+disease+caused+by+a+bacteria%3F&printsec=frontcover&source=bn&hl=en&ei=Khj-SZmdFaCltgegm62SDA&sa=X&oi=book_result&ct=result&resnum=4|Parkinson's Another Look]]
  
 {{tag>disease }} {{tag>disease }}
  
  
 +<nodisp>
 ===== Notes and comments ===== ===== Notes and comments =====
  
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 <blockquote>ASM Live 2011: Bacteria May Contribute to Development of Parkinsons Disease: A new mouse model suggests that the... bit.ly/iywhdJ</blockquote> <blockquote>ASM Live 2011: Bacteria May Contribute to Development of Parkinsons Disease: A new mouse model suggests that the... bit.ly/iywhdJ</blockquote>
-===== References =====+===== References =====</nodisp> 
home/diseases/parkinsons.1547159235.txt.gz · Last modified: 01.10.2019 by sallieq
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