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Correlations between peripheral blood mononuclear cell production of BDNF, TNF‐alpha, IL‐6, IL‐10 and cognitive performances in multiple sclerosis patients
Author(s) -
Patanella A.K.,
Zinno M.,
Quaranta D.,
Nociti V.,
Frisullo G.,
Gainotti G.,
Tonali P.A.,
Batocchi A.P.,
Marra C.
Publication year - 2010
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.22276
Subject(s) - peripheral blood mononuclear cell , brain derived neurotrophic factor , neuropsychology , cognition , multiple sclerosis , neurotrophic factors , tumor necrosis factor alpha , medicine , peripheral , interleukin , psychology , immunology , cytokine , psychiatry , biology , in vitro , biochemistry , receptor
The aim of this study was to investigate the role of Brain Derived Neurotrophic Factor (BDNF) and inflammatory factors in the development of cognitive dysfunctions in Multiple Sclerosis (MS). We correlated peripheral blood mononuclear cell (PBMC) production of BDNF, Tumor Necrosis Factor‐alpha (TNF‐α), Interleukin (IL)‐6 and IL‐10 with performances on specific neuropsychological tasks in a selected series of MS patients. We studied a sample of 30 patients with relapsing‐remitting (RR)MS, segregated by gender and matched for age, education, disease duration, type of immunomodulating therapy, degree of disability and overall cognitive status. We found that low BDNF levels were correlated with increased time of execution on a divided attention and visual scanning task whereas high levels of IL‐6 were correlated with low Mini Mental State Examination scores. We did not observe any significant correlations between IL‐10, TNF‐α levels and cognitive performances in our patients. In conclusion our study shows a correlation between low BDNF and high IL‐6 production by PBMCs and poorer performances in cognitive tasks in RRMS patients suggesting a possible role of these factors in cognitive impairment in MS. © 2009 Wiley‐Liss, Inc.