UK Researchers Apply for CFS “Diagnosis and Treatment” Patent

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UK Researchers Apply for CFS “Diagnosis and Treatment” Patent

10-18-2006

Dr. John W. Gow - a much-published neurobiologist who until recently led genetic research work on ME/CFS at the University of Glasgow in Scotland - has moved as of August 2006 to Glasgow Caledonian University, where he continues research addressing what he believes to be the unique “gene signature” of patients with ME/CFS.

The UK-based ME Association, a nonprofit organization that was instrumental in raising private-donor monies to support continuation of Dr. Gow’s research when its funding ran out, has encouraged donors to consider requesting that unspent donations be transferred to support his projects at Glasgow Caledonian University.

The patent application. Also in mid-August 2006, Dr. Gow and his fellow researcher at the University of Glasgow, Dr. Abhijit Chaudhuri, submitted an application to the European Patent Office for “a diagnostic tool for CFS.” The “invention” they wish to patent involves “materials and methods for diagnosis and treatment of CFS.” These are based on the genetic biomarkers for CFS that the two applicants have described in the course of their ongoing research – what they have termed “the gene signature” for ME/CFS.


The abstract of their application states:


The invention relates to materials and methods for diagnosis and treatment of chronic fatigue syndrome/myalgic encephalitis. A number of genes are identified which are expressed at abnormal levels in patients affected by CFS/ME as compared to normal healthy individuals. These genes include those encoding defensin a1, haemoglobin ?, CXCR4, tubulin beta 1, serine/threonine kinase 17B, HLA DRss4 and prostaglandin D2 synthase. The genes identified provide objective disease markers that may be used in diagnostic tests to support the diagnosis of CFS/ME or for monitoring the effectiveness of therapy. They also provide a rational basis for classifying CFS/ME patients according to the biochemical lesion [usually referring to a tissue abnormality] underlying their symptoms and enable provision of appropriate targeted therapies.

A very detailed description of the concepts underlying this patent application - complete with tables - is available at the European Patent Office Website.* But some key concepts seem to be that:
* The data produced by the materials and methods described might not by itself support “an absolute diagnosis of CFS,” but could help confirm or rule out a physician’s preliminary diagnosis based on physical or psychological symptoms.
*The idea is that if one or more of the genes the researchers have associated with CFS is “upregulated” - shows “at least a two-fold increase in expression” versus its expression in an unaffected individual – then a diagnosis of CFS would be likely. And if these genes are not upregulated, CFS might be ruled out.
*The doctors postulate that CFS is not a disease caused by inherited gene defects, but is an “acquired condition” involving changes in certain genes associated with infection, immunity, and “cell membrane function and cell cycle.”
* They believe they’ve observed what they call a “hub” and “network” relationship in the gene expression of CFS patients. The hub genes being like “control centers” and the network genes the hubs’ “implementers,” affecting a range of biological shifts or symptoms in CFS patients. Identification of different patterns might offer clues as to targeted therapies.

In reporting on this patent application, the CFIDS Association of America has noted that, because processing of patent applications averages four years in Europe, Drs. Gow and Chaudhuri will likely continue refining their knowledge – as will the other research groups involved in CFS genetic analysis around the world.
 
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