Founder of Health Rising and Phoenix Rising
Ha! It was the immune system - not the nervous system - that popped up in a gene expression study of FM. Interestingly given the Rituximab findings in ME/CFS B-cell development showed up in spades in FM. (Rituximab kills B-cells). Otherwise an immunodeficiency appeared present - an interesting finding give the results of the Lipkin/Hornig study....It's not too much immune activation perhaps - but not enough...
Biol Res Nurs. 2015 May 26. pii: 1099800415589785. [Epub ahead of print] Comparing Genomic Profiles of Women With and Without Fibromyalgia.Lukkahatai N1, Walitt B2, Espina A3, Wang D3, Saligan LN4.
Fibromyalgia syndrome (FMS), a chronic musculoskeletal condition characterized by diffuse pain, fatigue, sleep impairment, and cognitive dysfunction, is associated with significant functional disability. Its underlying biological mechanisms are unknown. This study investigated differentially expressed genes between women with FMS and healthy volunteers.
Women who met the 1990 or 2010 American College of Rheumatology fibromyalgia criteria were compared to age- and race-matched pain-free healthy women. Peripheral blood samples were collected, and a full genome microarray gene expression analysis was performed. One-way analysis of variance was used to identify differentially expressed genes using the filtering criterion of 1% false discovery rate. Analysis of canonical pathways associated with these genes was performed. Confirmatory quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay verified microarray results. Independent t-tests compared gene and protein expression between groups.
Participants were 54 women with FMS and 25 controls. Expression arrays from a subset of women with FMS (n = 29) and controls (n = 20) showed upregulation of 12 genes (>1.8-fold change, p < .05) in the FMS sample. Differentially expressed genes were related to B-cell development, primary immunodeficiency signaling, and mitotic roles of polo-like kinase. CENPK and HSP90AA1 were the most differentially expressed genes (p < .01).
Activity of interrelated pathways related to immune response, and homeostasis appears to be relevant to the experience of FMS. Replication and exploration of the relationship between gene expression and symptom severity will help determine clinical relevance of these findings.