La expresión génica diferencia SFC/EM de Depresión y Fibro
Publicado: 30 Jul 2015, 16:01
Este interesante estudio analizaba la expresión génica de unos determinados genes (34 genes), en enfermos de SFC, Fibromialgia, SFC+FM y Depresión contra controles sanos. Analizan los genes y los agrupan en 4 grupos que apenas se superponen, dividiéndolos por función 1) Moduladores de señales purinérgicas y celulares, 2) Crecimiento neuronal y función inmune, 3) Nocicepción y mediadores de estrés 4) Energía y función mitocondrial.
Curiosamente, los genes del grupo 1 y 3 se encontraron expresados en los enfermos de SFC y Depresión pero en sentido opuesto (aumentados en SFC/EM, disminuídos en Depresión), en cambio no en los de Fibromialgia (nota mía: eso demuestra que son enfermedades diferentes, no?)
Abstract
OBJECTIVE:
To determine if independent candidate genes can be grouped into meaningful biological factors and if these factors are associated with the diagnosis of chronic fatigue syndrome (CFS) and fibromyalgia (FMS) while controlling for co-morbid depression, sex, and age.
METHODS:
We included leukocyte mRNA gene expression from a total of 261 individuals including healthy controls (n=61), patients with FMS only (n=15), CFS only (n=33), co-morbid CFS and FMS (n=79), and medication-resistant (n=42) or medication-responsive (n=31) depression. We used Exploratory Factor Analysis (EFA) on 34 candidate genes to determine factor scores and regression analysis to examine if these factors were associated with specific diagnoses.
RESULTS:
EFA resulted in four independent factors with minimal overlap of genes between factors explaining 51% of the variance. We labeled these factors by function as: 1) Purinergic and cellular modulators; 2) Neuronal growth and immune function; 3) Nociception and stress mediators; 4) Energy and mitochondrial function. Regression analysis predicting these biological factors using FMS, CFS, depression severity, age, and sex revealed that greater expression in Factors 1 and 3 was positively associated with CFS and negatively associated with depression severity (QIDS score), but not associated with FMS.
CONCLUSION:
Expression of candidate genes can be grouped into meaningful clusters, and CFS and depression are associated with the same 2 clusters but in opposite directions when controlling for co-morbid FMS. Given high co-morbid disease and interrelationships between biomarkers, EFA may help determine patient subgroups in this population based on gene expression.
This article is protected by copyright. All rights reserved.© 2015, American College of Rheumatology.
PMID:
26097208
[PubMed - as supplied by publisher]
Curiosamente, los genes del grupo 1 y 3 se encontraron expresados en los enfermos de SFC y Depresión pero en sentido opuesto (aumentados en SFC/EM, disminuídos en Depresión), en cambio no en los de Fibromialgia (nota mía: eso demuestra que son enfermedades diferentes, no?)
Gene expression factor analysis to differentiate pathways linked to fibromyalgia, chronic fatigue syndrome, and depression in a diverse patient sample.
Iacob E , Light AR , Donaldson GW , Okifuji A , Hughen RW , White AT , Light KCAbstract
OBJECTIVE:
To determine if independent candidate genes can be grouped into meaningful biological factors and if these factors are associated with the diagnosis of chronic fatigue syndrome (CFS) and fibromyalgia (FMS) while controlling for co-morbid depression, sex, and age.
METHODS:
We included leukocyte mRNA gene expression from a total of 261 individuals including healthy controls (n=61), patients with FMS only (n=15), CFS only (n=33), co-morbid CFS and FMS (n=79), and medication-resistant (n=42) or medication-responsive (n=31) depression. We used Exploratory Factor Analysis (EFA) on 34 candidate genes to determine factor scores and regression analysis to examine if these factors were associated with specific diagnoses.
RESULTS:
EFA resulted in four independent factors with minimal overlap of genes between factors explaining 51% of the variance. We labeled these factors by function as: 1) Purinergic and cellular modulators; 2) Neuronal growth and immune function; 3) Nociception and stress mediators; 4) Energy and mitochondrial function. Regression analysis predicting these biological factors using FMS, CFS, depression severity, age, and sex revealed that greater expression in Factors 1 and 3 was positively associated with CFS and negatively associated with depression severity (QIDS score), but not associated with FMS.
CONCLUSION:
Expression of candidate genes can be grouped into meaningful clusters, and CFS and depression are associated with the same 2 clusters but in opposite directions when controlling for co-morbid FMS. Given high co-morbid disease and interrelationships between biomarkers, EFA may help determine patient subgroups in this population based on gene expression.
This article is protected by copyright. All rights reserved.© 2015, American College of Rheumatology.
PMID:
26097208
[PubMed - as supplied by publisher]