Synaptosomal-associated protein 25 (Snap-25) gene Polymorphism frequency in fibromyalgia syndrome and relationship with clinical symptoms

Abstract

BackgroundSNAP-25 protein is contributory to plasma membrane and synaptic vesicle fusions that are critical points in neurotransmission. SNAP-25 gene is associated with behavioral symptoms, personality and psychological disorders. In addition, SNAP-25 protein can be related to different neurotransmitter functions due to its association with vesicle membrane transition and fusion. This is important because neurologic, cognitive, and psychologic disorders in fibromyalgia syndrome (FMS) can be related to this function. This relationship may be enlightening for etiopathogenesis of FMS and treatment approaches. We aimed to study a SNAP-25 gene polymorphism, which is related to many psychiatric diseases, and FMS association in this prospective study.MethodsWe included 71 patients who were diagnosed according to new criteria and 57 matched healthy women in this study. Both groups were evaluated regarding age, height, weight, BMI, education level, marital and occupational status. A new diagnosis of FMS was made from criteria scoring, SF-36, Beck depression scale, and VAS that were applied to the patient group. SNAP-25 gene polymorphism and disease activity score correlations were compared.ResultsMean age was 38±5,196 and 38.12±4.939 in patient and control groups, respectively (p=0.542). No significant difference was found between groups regarding age, height, weight, BMI, education level, marital or occupational status (p > 0.05). Ddel T/C genotype was significantly higher in the patient group (p = 0.009). MnlI gene polymorphism did not show a correlation with any score whereas a significant correlation was found between Ddel T/C genotype and Beck depression scale and VAS score (p < 0.05).ConclusionFMS etiopathogenesis is not clearly known. Numerous neurologic, cognitive and psychological disorders were found during studies looking at cause. Our study showed increased SNAP-25 Ddel T/C genotype in FMS patients compared to the control group, which is related to behavioral symptoms, personality and psychological disorders in FMS patients.

Association of synaptosomal-associated protein 25 (SNAP-25) gene polymorphism with temperament and character traits in women with fibromyalgia syndrome

“…For this reason, SNAP-25 may be contributing to the pathogenesis of FMS by mediating the release of neurotransmitters such as serotonin and dopamine. In a study carried out by Balkarli et al 11 which was the preliminary of our study, it was reported that SNAP-25 gene polymorphism was more frequently detected in FMS. Depression and pain score was higher in patients with DdeI T/C genotype.…”

“…In a study of Balkarli et al 11 , it was found that SNAP-25 gene polymorphism was more frequently detected in FMS. Depression and pain score was higher in patients with DdeI T/C genotype.…”

Fatigue in Sjögren's Syndrome: A Search for Biomarkers and Treatment Targets

“…SNAP-25 protein is a SNARE protein, critical in neurotransmitter release (51). Aberrancies in this protein are described in several neurological, cognitive and psychological disorders like Alzheimer's disease and fibromyalgia (52–55). Also UCHL1 is particularly abundant in the brain, where it is critical for proper function of the ubiquitin-proteasome system in neurons (56).…”

Comparing Genomic Profiles of Women With and Without Fibromyalgia

“…While the pathways with increased gene products include glucocorticoid signaling and B-cell development, there has been no obvious pathologic dysfunction of these pathways noted in FMS. Rather than being an immunologic failing, the atypical B-cell findings appear to be another aspect of the organism-wide alterations in physiology noted in FMS, such as the reported alterations in pain processing, autonomic and neuroendocrine function, neurotransmitter concentrations, and small-fiber nerve density (Balkarli, Sengul, Tepeli, Balkarli, & Cobankara, 2014; Oaklander, Herzog, Downs, & Klein, 2013; Serra et al, 2014). Understanding the significance of these B-cell differences requires knowing whether such differences precede and predispose people to future symptom development, are causal in creating symptoms, or are just an epiphenomenon that accompanies or instantiates the experience of symptoms.…”