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   Author  Topic: CH history, genetic link and nicotine  (Read 15025 times)
Annette
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Re: CH history, genetic link and nicotine
« Reply #125 on: May 11th, 2008, 6:30am »
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on May 11th, 2008, 3:31am, MJ wrote:

 
Going from memory I believe first mentions of CH like symptoms were given in and about 7000 BC by some egyptian dude. Mention has been made of similarities from the times of the ancient aztecs in stories told through the ages. Of course they may have smoked. (I have no citations)
 
.

 
 
MJ
 
I have given a more personal reply in a PM to you.
 
On the thread though, since further information and discussion is good for the topic, would you be able to recall where you got that information ? Would you be able to find it again ?  
 
Thank you.
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Re: CH history, genetic link and nicotine
« Reply #126 on: May 12th, 2008, 11:54am »
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on May 10th, 2008, 6:57pm, Annette wrote:
Lee, would you have a transcript of what his colleague talked about last year? I know you said they havent found anything concrete, but at least was there any info on what they were looking at ? or looking for ? the hypothesis they were working on ?

I don't think a transcript exists, but this, I believe, is the latest published report in this respect:
 
Quote:
NEUROLOGY 2006;66:1888-1893
© 2006 American Academy of Neurology  
 
A genome-wide scan and HCRTR2 candidate gene analysis in a European cluster headache cohort
 
L. Baumber, BSc, C. Sjöstrand, MD, M. Leone, MD, H. Harty, BSc, G. Bussone, MD, J. Hillert, MD, PhD, R. C. Trembath, BSc, FRCP and M. B. Russell, MD, PhD, DMSci  
From the Division of Medical Genetics (L.B., H.H., R.C.T.), University of Leicester, UK; Department of Neurology (C.S., J.H.), Karolinska Institute, Karolinska University Hospital, Huddinge, Sweden; Carlo Besta National Neurological Institute (M.L., G.B.), Milan, Italy; Head and Neck Research Group, Akershus University Hospital, and Faculty Division, Akershus University Hospital (M.B.R.), University of Oslo, Norway; and Division of Medical & Molecular Genetics (L.B., R.C.T.), King’s College London (Guy’s Campus), Guy’s Hospital, London, UK.  
 
Address correspondence and reprint requests to Dr. Richard C. Trembath, Professor of Medical Genetics, Division of Medical & Molecular Genetics, King’s College London Medical School (Guy’s Campus), Floor 7, Guy’s Tower, Guy’s Hospital, London SE1 9RT, UK; e-mail: richard.trembath@genetics.kcl.ac.uk
 
Objective: To investigate the molecular genetic basis of cluster headache (CH), using a genome-wide scan and candidate gene strategy.  
 
Methods: Northern European CH families and a case-control cohort of Danish, Swedish, and British origin (total n = 259 sporadic CH patients), including 267 control subjects matched for ancestry, participated in the study. A genome-wide genetic screen using approximately 400 microsatellite markers was performed for five informative Danish CH families. Additional markers were typed for those loci generating statistical evidence suggestive of linkage, together with genotypes for 111 individuals from further Danish and Italian kindreds. Sporadic CH patients and controls were investigated by association analysis for variation in the candidate gene, HCRTR2. Finally, complete HCRTR2 sequencing was undertaken for eight independent probands.  
 
Results: Potential linkage was identified at four possible disease loci in Danish kindreds, yet no single chromosome location generated a lod or NPL score of recognized significance. No deleterious sequence variants of the HCRTR2 gene were detected by comparison to wild-type sequence. Association of the HCRTR2 gene was not replicated in this large dataset, even when the data were stratified into distinct populations.  
 
Conclusions: Cluster headache is a complex genetic disorder, with possible phenotypic and genetic heterogeneity compounding attempts at gene identification.

 
Full text here: http://www.neurology.org/cgi/content/full/66/12/1888
 
-Lee
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Re: CH history, genetic link and nicotine
« Reply #127 on: May 12th, 2008, 2:40pm »
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The original leanings of this thread were based on an this article from 2004
"A polymorphism of the hypocretin receptor 2 gene is associated with cluster headache."http://www.ncbi.nlm.nih.gov/pubmed/15477554
 
I believe this was first noted in 1999.
 
The theory seems to have been heavily contradicted  in further reading on the same site.
2007
"The G1246A polymorphism in the hypocretin receptor 2 gene is not associated with treatment response in cluster headache."
http://www.ncbi.nlm.nih.gov/pubmed/17376114?ordinalpos=1&itool=Entre zSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=2&log$=relatedarticles&dbfrom=pubmed
 
2007
The 1246G-->A polymorphism of the HCRTR2 gene is not associated with migraine. or clusters
http://www.ncbi.nlm.nih.gov/pubmed/17645762?ordinalpos=1&itool=Entre zSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=5&log$=relatedarticles&dbfrom=pubmed
 
From LeeS link
2006
"Association of the HCRTR2 gene was not replicated in this large dataset, even when the data were stratified into distinct populations"
 
 
Goes to show what we think today may not be true tommorrow and what we want tommorrow we can find from yesterday.
The science of the mind is an ever changing art.
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Re: CH history, genetic link and nicotine
« Reply #128 on: May 12th, 2008, 4:43pm »
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MJ,
 
Please read the articles in full if you can.
 
The 1st article about polymorphism for the gene not corresponding to treatment : the final result is that although people have the genes, they dont respond to the same meds the same way. It simply means there are other factors influencing their CH. It doesnt mean the gene is not associated with CH.
 
The 2nd article says that the same gene that was found to be associated with CH is not found to be associated with migraine. Although migraine is very close to CH but genetically its a different entity all together.
 
The 3rd article tested a larger population of CHers and found that the majority does not have this gene and still have CH. It simply means people can develop CH via other mechanisms.
 
All in all, they do not discount the fact that the gene has been found to be associated with CH. They just showed that CH is much more complicated than one allele of the gene.  
 
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Re: CH history, genetic link and nicotine
« Reply #129 on: May 13th, 2008, 2:51am »
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Quote:


 
Headache. April 2008, Online first:
 
Haplotype Analysis Confirms the Association Between the HCRTR2 Gene and Cluster Headache.
 
Rainero I, Gallone S, Rubino E, Ponzo P, Valfre W, Binello E, Fenoglio P, Gentile S, Anoaica M, Gasparini M, Pinessi L.
 
Neurology II—Headache Center—Department of Neuroscience, Turin, Italy.
 
Background.- Several studies suggested that genetic factors play a role in cluster headache (CH) susceptibility. We found a significant association between the 1246 G>A polymorphism of the hypocretin receptor-2 (HCRTR2) gene and the disease. This association was confirmed in a large study from Germany but was not replicated in a dataset of CH patients from Northern Europe. Objective.- The purpose of this study was to further evaluate the association between CH and the HCRTR2 gene using new polymorphisms, estimating the frequency of different gene haplotypes, searching for gene mutations, and evaluating the effects of the examined polymorphisms on hypocretin binding sites.  
 
Methods.- We genotyped 109 CH patients and 211 healthy controls for 5 new polymorphisms of the HCRTR2 gene and we inferred different gene haplotypes. Complete HCRTR2 sequencing was undertaken for 11 independent CH patients, 5 of whom had a positive family history. The effects of the 1246 G>A polymorphism on the hypocretin binding sites were evaluated using different computer-assisted analyses. Results.- Three new polymorphisms of the HCRTR2 gene resulted significantly associated with CH. The GTAAGG haplotype resulted more frequent in cases than in controls (OR: 3.68; 95% CI: 1.85-7.67). No point mutation of the HCRTR2 gene was found. Binding analyses showed that the 1246 G>A polymorphism (substitution of valine at position 308 by isoleucine) has no effect on the hypocretin binding sites but could influence the dimerization process of the receptor.  
 
Conclusion.- Our data confirm previous studies suggesting that the HCRTR2 gene or a linked locus significantly modulates the risk for CH. In addition, we suggest that the V308I substitution of the HCRTR2 may interfere with the dimerization process of the receptor, thereby influencing its functional activity.
 
PMID: 18399985
 
Source: http://www.ncbi.nlm.nih.gov/pubmed/18399985?ordinalpos=1&itool=Entre zSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

 

 
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