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Thread: Diagnostic Test for Idiopathic Scoliosis

  1. #16
    Join Date
    Jan 2006
    Houston TX

    Genetic test

    I am always skeptical of researchers who have a press release before they can even disclose what gene that they are studying.

    The current publication by Dr. Moreau only gives clues that it may be related to melatonin (a hormone that regulates wake/sleep patterns) biology. Even if there is a genetic relationship, there is no data the would support why or how this genetic variation results in scoliosis. This means that this group has at least 10-15 years research until the diagnosis can be used to preventively treat scoliosis.

    The only publication by Dr. Moreau is the following:

    Spine. 2004 Aug 15;29(16):1772-81.
    Melatonin signaling dysfunction in adolescent idiopathic scoliosis.

    Moreau A, Wang da S, Forget S, Azeddine B, Angeloni D, Fraschini F, Labelle H, Poitras B, Rivard CH, Grimard G.

    Research Center, Sainte-Justine Hospital, Bone Molecular Genetics and Musculoskeletal Malformations Laboratory, Montreal, Quebec, Canada.

    STUDY DESIGN: In vitro assays were performed with bone-forming cells isolated from 41 patients with adolescent idiopathic scoliosis and 17 control patients exhibiting another type of scoliosis or none. OBJECTIVE: To determine whether a dysfunction of the melatonin-signaling pathway in tissues targeted by this hormone is involved in adolescent idiopathic scoliosis. SUMMARY OF BACKGROUND DATA: Pinealectomy in chicken has led to the formation of a scoliotic deformity, thereby suggesting that a melatonin deficiency may be at the source of adolescent idiopathic scoliosis. However, the relevance of melatonin in the etiopathogenesis of that condition is controversial because most studies have reported no significant change in circulating levels of melatonin in patients with adolescent idiopathic scoliosis. METHODS: Primary osteoblast cultures prepared from bone specimens obtained intraoperatively during spine surgeries were used to test the ability of melatonin and Gpp(NH)p, a GTP analogue, to block cAMP accumulation induced by forskolin. In parallel, melatonin receptor and Gi protein functions were evaluated by immunohistochemistry and by coimmunoprecipitation experiments. RESULTS: The cAMP assays demonstrated that melatonin signaling was impaired in osteoblasts isolated from adolescent idiopathic scoliosis patients to different degrees allowing their classification in 3 distinct groups based on their responsiveness to melatonin or Gpp(NH)p. CONCLUSION: Melatonin signaling is clearly impaired in osteoblasts of all patients with adolescent idiopathic scoliosis tested. Classification of patients with adolescent idiopathic scoliosis in 3 groups based on functional in vitro assays suggests the presence of distinct mutations interfering with the melatonin signal transduction. Posttranslational modifications affecting Gi protein function, such as serine residues phosphorylation, should be considered as one possible mechanism in the etiopathogenesis of AIS.
    Melatonin signaling dysfunction in adolescent idiopathic scoliosis.

  2. #17
    Join Date
    Apr 2005
    That's intersting to say the least, from what I did understand. I'm the world's biggest insomniac and have been since I was a child. I did try Melatonin and it gave me nightmares.
    35 y/old female from Montreal, Canada
    Diagnosed with scoliosis(double major) at age 12, wore Boston brace 4 years at least 23 hours a day-curve progressed
    Surgery age 26 for 60 degree curve in Oct. 1997 by Dr.Max Aebi-fused T5 to L2
    Surgery age 28 for a hook removal in Feb. 1999 by Dr.Max Aebi-pain free for 5 years
    Surgery age 34 in Dec.2005 for broken rod replacement, bigger screws and crosslinks added and pseudarthrosis(non union) by Dr. Jean Ouellet

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