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For: Hamed SA, Selim ZI, Elattar AM, Elserogy YM, Ahmed EA, Mohamed HO. Assessment of biocorrelates for brain involvement in female patients with rheumatoid arthritis. Clin Rheumatol 2011;31:123-32. [PMID: 21695659 DOI: 10.1007/s10067-011-1795-1] [Citation(s) in RCA: 38] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/04/2010] [Revised: 06/01/2011] [Accepted: 06/05/2011] [Indexed: 12/22/2022]

For:	Hamed SA, Selim ZI, Elattar AM, Elserogy YM, Ahmed EA, Mohamed HO. Assessment of biocorrelates for brain involvement in female patients with rheumatoid arthritis. Clin Rheumatol 2011;31:123-32. [PMID: 21695659 DOI: 10.1007/s10067-011-1795-1] [Citation(s) in RCA: 38] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/04/2010] [Revised: 06/01/2011] [Accepted: 06/05/2011] [Indexed: 12/22/2022]

Number

Cited by Other Article(s)

Pankowski D, Wytrychiewicz-Pankowska K, Pisula E, Fal AM. Prevalence of neurocognitive impairment in patients with rheumatoid arthritis - a systematic review and meta-analysis. Clin Neuropsychol 2025;39:252-272. [PMID: 39086212 DOI: 10.1080/13854046.2024.2378521] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/27/2024] [Accepted: 07/06/2024] [Indexed: 08/02/2024]

Kim JI, Kang B. A comparative retrospective longitudinal study of arthritis risk and cognitive decline in older adults. Sci Rep 2024;14:24739. [PMID: 39433863 PMCID: PMC11494171 DOI: 10.1038/s41598-024-75774-7] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/26/2024] [Accepted: 10/08/2024] [Indexed: 10/23/2024] Open

Fradera A, McLaren J, Gadon L, Cullen B, Evans J. Does the presence of chronic pain affect scores on cognitive screening tests/brief cognitive measures for dementia? A systematic review and meta-analysis. Clin Neuropsychol 2024;38:1586-1609. [PMID: 38369508 DOI: 10.1080/13854046.2024.2315739] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/21/2023] [Accepted: 12/27/2023] [Indexed: 02/20/2024]

Fan KQ, Huang T, Yu JS, Li YY, Jin J. The clinical features and potential mechanisms of cognitive disorders in peripheral autoimmune and inflammatory diseases. FUNDAMENTAL RESEARCH 2024;4:226-236. [PMID: 38933510 PMCID: PMC11197673 DOI: 10.1016/j.fmre.2022.12.005] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/18/2022] [Revised: 10/15/2022] [Accepted: 12/05/2022] [Indexed: 12/26/2022] Open

Duan L, Li S, Li H, Shi Y, Xie X, Feng Y. Causality between rheumatoid arthritis and the risk of cognitive impairment: a Mendelian randomization study. Arthritis Res Ther 2024;26:5. [PMID: 38167504 PMCID: PMC10759661 DOI: 10.1186/s13075-023-03245-x] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/16/2023] [Accepted: 12/18/2023] [Indexed: 01/05/2024] Open

Sousa DCD, de Almeida SB, Roriz Filho JDS, Freitas TH, Braga-Neto P. Cognitive Dysfunction Biomarkers in Patients With Rheumatoid Arthritis: A Systematic Review. J Clin Rheumatol 2023;29:159-164. [PMID: 36729842 DOI: 10.1097/rhu.0000000000001888] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/03/2023]

Abstract

BACKGROUND/OBJECTIVES

During the last years, a growing number of studies have investigated the link between cognitive dysfunction and rheumatoid arthritis (RA), highlighting the potential pathogenic role of several clinical, psychological, and biological factors. We aimed to investigate serological and cerebrospinal fluid biomarkers in humans and its association with cognitive dysfunction in patients with RA.

METHODS

We performed a systematic review using PRISMA (Preferred Reported Items for Systematic Reviews and Meta-analysis) protocol. A systematic search was conducted in the PubMed/MEDLINE, EMBASE, LILACS, Scopus, and Google Scholar databases from inception up to November 2021. The inclusion criteria for studies were defined based on the participants involved, type of exposure, type of comparison group, outcome of interest, and study design.

RESULTS

Five original studies were included, which provided data from 428 participants. Among plasma proteins, SHH was increased and TTR was reduced in patients with mild cognitive impairment; anti-myelin basic protein and anti-myelin oligodendrocyte glycoprotein negatively correlated with memory, executive function, and attention. S100β negatively correlated with memory and executive functions; some lymphocyte subpopulations positively correlated with attention, memory, and executive functions. Interleukin 2 [IL-2], IL-4, IL-6, and tumor necrosis factor α negatively correlated with memory and positively correlated with executive functions. Interleukin 1β negatively correlated with global cognitive dysfunction and positively correlated with logical thinking. Interleukin 10 and brain-derived neurotrophic factor negatively correlated with memory.

CONCLUSION

Despite the relative scarcity of studies on this subject and the heterogeneity of results, we identified possible biomarkers for cognitive deficits in the RA population. Further longitudinal studies are warranted to clarify these associations and the establishment of possible biomarkers for cognitive deficits in RA.

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Mena-Vázquez N, Ortiz-Márquez F, Cabezudo-García P, Padilla-Leiva C, Diaz-Cordovés Rego G, Muñoz-Becerra L, Ramírez-García T, Lisbona-Montañez JM, Manrique-Arija S, Mucientes A, Núñez-Cuadros E, Galindo Zavala R, Serrano-Castro PJ, Fernández-Nebro A. Longitudinal Study of Cognitive Functioning in Adults with Juvenile Idiopathic Arthritis. Biomedicines 2022;10:biomedicines10071729. [PMID: 35885032 PMCID: PMC9312867 DOI: 10.3390/biomedicines10071729] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/08/2022] [Revised: 07/14/2022] [Accepted: 07/15/2022] [Indexed: 11/16/2022] Open

Abstract

Objective: To prospectively evaluate possible decline of cognitive functions in adult patients with juvenile idiopathic arthritis (JIA) and identify associated factors. Patients and methods: We performed a 24-month prospective observational study of adults (≥16 years) with JIA. The primary outcome measure was decline in cognitive function defined as a worsening of ≥2 points on the scales of the subsets administered to evaluate the different cognitive areas using the Wechsler Adult Intelligence Scale (WAIS) after 24 months: attention/concentration (digit span); verbal function (vocabulary); visual-spatial organization (block design); working memory (letter-number sequencing); and problem solving (similarities). Other variables included average inflammatory activity using C-reactive protein and composite activity indexes, comorbidity, and treatment. Logistic regression was performed to identify factors associated with cognitive decline. Results: The study population comprised 52 patients with JIA. Of these, 15 (28.8%) had cognitive decline at V24. The most affected functions were working memory (17.3%), attention/concentration (9.6%), verbal function (7.7%), visual-spatial organization (7.7%), and problem solving (3.8%). There were no significant differences in the median direct or scale scores for the cognitive functions evaluated between V0 and V24 for the whole sample. The factors associated with cognitive decline in patients with JIA were average C-reactive protein (OR [95% CI], 1.377 [1.060–1.921]; p = 0.039), depression (OR [95% CI], 3.691 [1.294–10.534]; p = 0.015), and treatment with biologics (OR [95% CI], 0.188 [0.039–0.998]; p = 0.046). Conclusion: Cognitive decline was detected in almost one third of adults with JIA after 24 months of follow-up. Systemic inflammatory activity in JIA patients was related to cognitive decline. Patients treated with biologics had a lower risk of decline in cognitive functions.

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Affiliation(s)

Natalia Mena-Vázquez Instituto de Investigación Biomedica de Málaga (IBIMA)-Plataforma Bionand, 29010 Malaga, Spain; (N.M.-V.); (F.O.-M.); (G.D.-C.R.); (L.M.-B.); (T.R.-G.); (J.M.L.-M.); (S.M.-A.); (A.M.); (E.N.-C.); (R.G.Z.); (P.J.S.-C.); (A.F.-N.) Unidad de Gestion Clinica de Reumatología, Hospital Regional Universitario de Málaga, 29009 Malaga, Spain
Fernando Ortiz-Márquez Instituto de Investigación Biomedica de Málaga (IBIMA)-Plataforma Bionand, 29010 Malaga, Spain; (N.M.-V.); (F.O.-M.); (G.D.-C.R.); (L.M.-B.); (T.R.-G.); (J.M.L.-M.); (S.M.-A.); (A.M.); (E.N.-C.); (R.G.Z.); (P.J.S.-C.); (A.F.-N.) Unidad de Gestion Clinica de Reumatología, Hospital Regional Universitario de Málaga, 29009 Malaga, Spain
Pablo Cabezudo-García Instituto de Investigación Biomedica de Málaga (IBIMA)-Plataforma Bionand, 29010 Malaga, Spain; (N.M.-V.); (F.O.-M.); (G.D.-C.R.); (L.M.-B.); (T.R.-G.); (J.M.L.-M.); (S.M.-A.); (A.M.); (E.N.-C.); (R.G.Z.); (P.J.S.-C.); (A.F.-N.) Servicio de Neurología, Unidad de Gestion Clinica de Neurociencias, Hospital Regional Universitario de Malaga (HRUM), 29010 Malaga, Spain Correspondence: ; Tel.: +34-951291135
Claudia Padilla-Leiva Departamento de Medicina, Universidad de Málaga, 29016 Malaga, Spain;
Gisela Diaz-Cordovés Rego Instituto de Investigación Biomedica de Málaga (IBIMA)-Plataforma Bionand, 29010 Malaga, Spain; (N.M.-V.); (F.O.-M.); (G.D.-C.R.); (L.M.-B.); (T.R.-G.); (J.M.L.-M.); (S.M.-A.); (A.M.); (E.N.-C.); (R.G.Z.); (P.J.S.-C.); (A.F.-N.) Unidad de Gestion Clinica de Reumatología, Hospital Regional Universitario de Málaga, 29009 Malaga, Spain
Luis Muñoz-Becerra Instituto de Investigación Biomedica de Málaga (IBIMA)-Plataforma Bionand, 29010 Malaga, Spain; (N.M.-V.); (F.O.-M.); (G.D.-C.R.); (L.M.-B.); (T.R.-G.); (J.M.L.-M.); (S.M.-A.); (A.M.); (E.N.-C.); (R.G.Z.); (P.J.S.-C.); (A.F.-N.) Servicio de Neurología, Unidad de Gestion Clinica de Neurociencias, Hospital Regional Universitario de Malaga (HRUM), 29010 Malaga, Spain
Teresa Ramírez-García Instituto de Investigación Biomedica de Málaga (IBIMA)-Plataforma Bionand, 29010 Malaga, Spain; (N.M.-V.); (F.O.-M.); (G.D.-C.R.); (L.M.-B.); (T.R.-G.); (J.M.L.-M.); (S.M.-A.); (A.M.); (E.N.-C.); (R.G.Z.); (P.J.S.-C.); (A.F.-N.) Servicio de Neurología, Unidad de Gestion Clinica de Neurociencias, Hospital Regional Universitario de Malaga (HRUM), 29010 Malaga, Spain
Jose Manuel Lisbona-Montañez Instituto de Investigación Biomedica de Málaga (IBIMA)-Plataforma Bionand, 29010 Malaga, Spain; (N.M.-V.); (F.O.-M.); (G.D.-C.R.); (L.M.-B.); (T.R.-G.); (J.M.L.-M.); (S.M.-A.); (A.M.); (E.N.-C.); (R.G.Z.); (P.J.S.-C.); (A.F.-N.) Unidad de Gestion Clinica de Reumatología, Hospital Regional Universitario de Málaga, 29009 Malaga, Spain Departamento de Medicina, Universidad de Málaga, 29016 Malaga, Spain;
Sara Manrique-Arija Instituto de Investigación Biomedica de Málaga (IBIMA)-Plataforma Bionand, 29010 Malaga, Spain; (N.M.-V.); (F.O.-M.); (G.D.-C.R.); (L.M.-B.); (T.R.-G.); (J.M.L.-M.); (S.M.-A.); (A.M.); (E.N.-C.); (R.G.Z.); (P.J.S.-C.); (A.F.-N.) Unidad de Gestion Clinica de Reumatología, Hospital Regional Universitario de Málaga, 29009 Malaga, Spain Departamento de Medicina, Universidad de Málaga, 29016 Malaga, Spain;
Arkaitz Mucientes Instituto de Investigación Biomedica de Málaga (IBIMA)-Plataforma Bionand, 29010 Malaga, Spain; (N.M.-V.); (F.O.-M.); (G.D.-C.R.); (L.M.-B.); (T.R.-G.); (J.M.L.-M.); (S.M.-A.); (A.M.); (E.N.-C.); (R.G.Z.); (P.J.S.-C.); (A.F.-N.) Unidad de Gestion Clinica de Reumatología, Hospital Regional Universitario de Málaga, 29009 Malaga, Spain
Esmeralda Núñez-Cuadros Instituto de Investigación Biomedica de Málaga (IBIMA)-Plataforma Bionand, 29010 Malaga, Spain; (N.M.-V.); (F.O.-M.); (G.D.-C.R.); (L.M.-B.); (T.R.-G.); (J.M.L.-M.); (S.M.-A.); (A.M.); (E.N.-C.); (R.G.Z.); (P.J.S.-C.); (A.F.-N.) Unidad de Gestion Clinica de Pediatría, Hospital Regional Universitario de Málaga, 29009 Malaga, Spain
Rocío Galindo Zavala Instituto de Investigación Biomedica de Málaga (IBIMA)-Plataforma Bionand, 29010 Malaga, Spain; (N.M.-V.); (F.O.-M.); (G.D.-C.R.); (L.M.-B.); (T.R.-G.); (J.M.L.-M.); (S.M.-A.); (A.M.); (E.N.-C.); (R.G.Z.); (P.J.S.-C.); (A.F.-N.) Unidad de Gestion Clinica de Pediatría, Hospital Regional Universitario de Málaga, 29009 Malaga, Spain
Pedro Jesús Serrano-Castro Instituto de Investigación Biomedica de Málaga (IBIMA)-Plataforma Bionand, 29010 Malaga, Spain; (N.M.-V.); (F.O.-M.); (G.D.-C.R.); (L.M.-B.); (T.R.-G.); (J.M.L.-M.); (S.M.-A.); (A.M.); (E.N.-C.); (R.G.Z.); (P.J.S.-C.); (A.F.-N.) Servicio de Neurología, Unidad de Gestion Clinica de Neurociencias, Hospital Regional Universitario de Malaga (HRUM), 29010 Malaga, Spain Departamento de Medicina, Universidad de Málaga, 29016 Malaga, Spain;
Antonio Fernández-Nebro Instituto de Investigación Biomedica de Málaga (IBIMA)-Plataforma Bionand, 29010 Malaga, Spain; (N.M.-V.); (F.O.-M.); (G.D.-C.R.); (L.M.-B.); (T.R.-G.); (J.M.L.-M.); (S.M.-A.); (A.M.); (E.N.-C.); (R.G.Z.); (P.J.S.-C.); (A.F.-N.) Unidad de Gestion Clinica de Reumatología, Hospital Regional Universitario de Málaga, 29009 Malaga, Spain Departamento de Medicina, Universidad de Málaga, 29016 Malaga, Spain;

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Phukan P, Barman B, Chengappa NK, Lynser D, Paul S, Nune A, Sarma K. Diffusion tensor imaging analysis of rheumatoid arthritis patients with neuropsychiatric features to determine the alteration of white matter integrity due to vascular events. Clin Rheumatol 2022;41:3169-3177. [PMID: 35751734 DOI: 10.1007/s10067-022-06262-4] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/11/2022] [Revised: 06/19/2022] [Accepted: 06/20/2022] [Indexed: 11/27/2022]

Abstract

INTRODUCTION

The pathophysiology of neuropsychiatric manifestations in rheumatoid arthritis is not well known. The magnetic resonance imaging of the brain in rheumatoid arthritis demonstrates non-specific findings, and in the majority of cases, magnetic resonance imaging fails to detect an abnormality, even in rheumatoid arthritis patients with neuropsychiatric manifestations. Therefore, we aimed to assess microstructural integrity changes of white matter in patients with rheumatoid arthritis by using different diffusion tensor imaging parameters.

METHODS

Eighteen rheumatoid arthritis patients (10 with neuropsychiatric symptoms and 8 without any neuropsychiatric symptoms) and 14 controls were included. The volume of the T2 hyperintense lesions was assessed. Different diffusion tensor imaging parameters such as fractional anisotropy, apparent diffusion coefficient, trace, axial diffusivity, and radial diffusivity were obtained from six different regions of white matter. Inter group significant difference was determined by one-way analysis of variance followed by Tukey's post hoc test. The accuracy of diffusion tensor imaging matrices was evaluated from the receiver operating characteristic curve.

RESULTS

No significant difference in lesions' volume was detected between rheumatoid arthritis patients with or without neuropsychiatric symptoms. There was an increased apparent diffusion coefficient and radial diffusivity (p < 0.05) as well as decreased fractional anisotropy and axial diffusivity (p < 0.5) in rheumatoid arthritis patients with neuropsychiatric symptoms compared to controls. Moreover, the apparent diffusion coefficient (p < .05) was increased in both positive and negative MRI of patients with neuropsychiatric features compared to the control group. The sensitivity and specificity of the apparent diffusion coefficient parameters was 73% and 72%, respectively.

CONCLUSIONS

The various anisotropic metrics were altered in rheumatoid arthritis patients with neuropsychiatric symptoms by using diffusion tensor imaging analysis, representing that central nervous system vasculitis leads to tissue hypoxia resulting in vasogenic edema. This may lead to axonal and myelin degeneration of white matter fibers and neuronal cell disruption. Key Points • Our study confirms that neurovascular events are not uncommon in RA patients with NP features. Diffusion tensor imaging (DTI) is superior to conventional MRI scan for RA patients with NP features because it distinguishes between gray and white matter structures. • RA patients with NP features are more likely to have microstructural changes detected by DTI than by DWI, and it can provide comprehensive anatomical layouts describing regional disparities in neurodegeneration. • DTI's quantitative association of NP symptoms in a large patient cohort is an important study scope.

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Pankowski D, Wytrychiewicz-Pankowska K, Janowski K, Pisula E. Cognitive impairment in patients with rheumatoid arthritis: A systematic review and meta-analysis. Joint Bone Spine 2021;89:105298. [PMID: 34656753 DOI: 10.1016/j.jbspin.2021.105298] [Citation(s) in RCA: 10] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/07/2021] [Revised: 09/16/2021] [Accepted: 10/06/2021] [Indexed: 12/31/2022]

Basile MS, Ciurleo R, Bramanti A, Petralia MC, Fagone P, Nicoletti F, Cavalli E. Cognitive Decline in Rheumatoid Arthritis: Insight into the Molecular Pathogenetic Mechanisms. Int J Mol Sci 2021;22:ijms22031185. [PMID: 33530359 PMCID: PMC7865873 DOI: 10.3390/ijms22031185] [Citation(s) in RCA: 20] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/28/2020] [Revised: 01/19/2021] [Accepted: 01/22/2021] [Indexed: 12/21/2022] Open

Steiner GZ, Barry RJ, Wassink K, De Blasio FM, Fogarty JS, Cave AE, Love S, Armour M. Neuronal Correlates of Cognitive Control Are Altered in Women With Endometriosis and Chronic Pelvic Pain. Front Syst Neurosci 2020;14:593581. [PMID: 33390910 PMCID: PMC7772245 DOI: 10.3389/fnsys.2020.593581] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/11/2020] [Accepted: 11/11/2020] [Indexed: 12/13/2022] Open

Ingegnoli F, Buoli M, Antonucci F, Coletto LA, Esposito CM, Caporali R. The Link Between Autonomic Nervous System and Rheumatoid Arthritis: From Bench to Bedside. Front Med (Lausanne) 2020;7:589079. [PMID: 33365319 PMCID: PMC7750536 DOI: 10.3389/fmed.2020.589079] [Citation(s) in RCA: 26] [Impact Index Per Article: 5.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/30/2020] [Accepted: 10/30/2020] [Indexed: 12/25/2022] Open

Mena-Vázquez N, Cabezudo-García P, Ortiz-Márquez F, Díaz-Cordovés Rego G, Muñoz-Becerra L, Manrique-Arija S, Fernández-Nebro A. Evaluation of cognitive function in adult patients with juvenile idiopathic arthritis. Int J Rheum Dis 2020;24:81-89. [PMID: 33112486 DOI: 10.1111/1756-185x.14009] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/18/2020] [Revised: 09/08/2020] [Accepted: 10/04/2020] [Indexed: 11/27/2022]

Barbé-Tuana F, Funchal G, Schmitz CRR, Maurmann RM, Bauer ME. The interplay between immunosenescence and age-related diseases. Semin Immunopathol 2020;42:545-557. [PMID: 32747977 PMCID: PMC7398288 DOI: 10.1007/s00281-020-00806-z] [Citation(s) in RCA: 173] [Impact Index Per Article: 34.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/15/2020] [Accepted: 07/06/2020] [Indexed: 02/07/2023]

Bauer ME. Accelerated immunosenescence in rheumatoid arthritis: impact on clinical progression. IMMUNITY & AGEING 2020;17:6. [PMID: 32190092 PMCID: PMC7068869 DOI: 10.1186/s12979-020-00178-w] [Citation(s) in RCA: 61] [Impact Index Per Article: 12.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 12/25/2019] [Accepted: 03/04/2020] [Indexed: 02/07/2023]

Extracellular Vesicles from Hyperammonemic Rats Induce Neuroinflammation and Motor Incoordination in Control Rats. Cells 2020;9:cells9030572. [PMID: 32121257 PMCID: PMC7140428 DOI: 10.3390/cells9030572] [Citation(s) in RCA: 11] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/11/2020] [Revised: 02/24/2020] [Accepted: 02/25/2020] [Indexed: 12/12/2022] Open

Sağ S, Sağ MS, Tekeoğlu I, Kamanlı A, Nas K, Acar BA. Central nervous system involvement in rheumatoid arthritis: possible role of chronic inflammation and tnf blocker therapy. Acta Neurol Belg 2020;120:25-31. [PMID: 29288410 DOI: 10.1007/s13760-017-0879-3] [Citation(s) in RCA: 13] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/13/2017] [Accepted: 12/26/2017] [Indexed: 12/29/2022]

Abstract

Rheumatoid arthritis (RA) is a chronic disease, the etiology of which has yet to be clarified, which causes activation of proinflammatory pathways that bring about joint and systemic inflammation. Although peripheral nervous system anomalies are observed widely in RA, very few case reports on changes in the central nervous system (CNS) have been published. In recent years, the pathophysiology of CNS involvement that can occur in RA has attracted a great deal of attention. Emphasis has focused on the possibility that CNS involvement occurs due to blood-brain barrier (BBB) damage associated with chronic inflammation. The present study was performed to investigate the possible effects of BBB dysfunction and tumor necrosis factor (TNF) blocker therapy on BBB function, which may cause CNS damage in patients with RA. 58 RA patients [47 (81.0%) females, 11 (19.0%) males] and 34 healthy controls [24 (70.6%) females, 10 (29.4%) males] were included in the study. All RA patients were on synthetic DMARD therapy at the beginning. Thirty patients continued DMARD therapy, and 28 patients with high disease activity were started on TNF blocker therapy. All demographic characteristics of the patients were recorded. Disease activity was evaluated using the Disease Activity Score 28-joint count C reactive protein. The Mini-Mental State Examination was used to evaluate cognitive function, and the Fazekas scale was used to assess cranial lesions visualized by magnetic resonance imaging (MRI). Patients' peripheral blood S100β, glial fibrillary acidic protein (GFAP), claudin, interleukin (IL)-17, and IL-1β levels were measured at the beginning of the study and after 6 months. Demographic characteristics (including sex, age, and body mass index) were similar in the RA and control groups. S100β and GFAP levels were significantly higher in the patient group than in the control group. In the group that was started on TNF blocker therapy, S100β and GFAP levels were significantly decreased 6 months after commencement of treatment. No difference was observed between the RA and control groups in terms of hyperintense lesions seen on cranial MRI. The S100β levels increased with lesions in the deep white matter seen on cranial MRI in patients with RA. In conclusion, next to decreasing disease activity and joint erosions by suppressing inflammation, anti-TNF therapy in RA can also suppress potential CNS involvement linked to BBB (blood-brain barrier) dysfunction. Further studies with broader participation and longer patient follow-up are needed to reinforce this hypothesis.

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Tokdemir S, Toprak H, Alkan A. Unusual Cerebral Involvement of Rheumatoid Arthritis Mimicking a Tumor. Curr Med Imaging 2020;16:145-148. [PMID: 32003314 DOI: 10.2174/1573405614666180911121222] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/10/2018] [Revised: 08/09/2018] [Accepted: 08/19/2018] [Indexed: 11/22/2022]

Borren NZ, van der Woude CJ, Ananthakrishnan AN. Fatigue in IBD: epidemiology, pathophysiology and management. Nat Rev Gastroenterol Hepatol 2019;16:247-259. [PMID: 30531816 DOI: 10.1038/s41575-018-0091-9] [Citation(s) in RCA: 156] [Impact Index Per Article: 26.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]

S100 proteins in rheumatic diseases. Nat Rev Rheumatol 2018;14:528-541. [DOI: 10.1038/s41584-018-0058-9] [Citation(s) in RCA: 76] [Impact Index Per Article: 10.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/22/2022]

Proteomic analysis of plasma from rheumatoid arthritis patients with mild cognitive impairment. Clin Rheumatol 2018. [PMID: 29525843 DOI: 10.1007/s10067-017-3974-1] [Citation(s) in RCA: 14] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/21/2022]

Petersen LE, Baptista TSA, Molina JK, Motta JG, do Prado A, Piovesan DM, de Nardi T, Viola TW, Vieira ÉLM, Teixeira AL, Grassi-Oliveira R, Bauer ME. Cognitive impairment in rheumatoid arthritis: role of lymphocyte subsets, cytokines and neurotrophic factors. Clin Rheumatol 2018;37:1171-1181. [PMID: 29372349 DOI: 10.1007/s10067-018-3990-9] [Citation(s) in RCA: 35] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/14/2017] [Revised: 01/11/2018] [Accepted: 01/15/2018] [Indexed: 11/08/2022]

Abstract

To what extent the cognitive impairment of rheumatoid arthritis (RA) is modulated by autoimmune and/or inflammatory activity is largely unknown. The aim of this study was to investigate the role of peripheral inflammation on cognitive functions of patients with active (Ac-), controlled (Co-) RA and healthy controls. In a cross-sectional study, 102 RA patients and 30 matched healthy controls were recruited. B and T cell subsets were immunophenotyped by flow cytometry. Plasma cytokines and neurotrophins were measured by flow cytometry and ELISA, respectively. Cognitive performance, depression and stress were evaluated by structured clinical interviews. Generalized linear modeling (GzLM) was used to compare differences between groups and multiple linear regression models were used to explore the predictive value of immune variables on cognitive performance. RA patients had overall cognitive impairment. Of note, the Ac-RA had the poorest performance on digit span (DST) and N-back when compared to Co-RA and control group (DST 9.9 ± 2.1, 12.9 ± 4.2, 15.5 ± 4.7, respectively; N-back 49.2 ± 8.3, 55.5 ± 11.1, 60.8 ± 9.1, respectively, all p < 0.0001). RA patients had expansions of immature B cells (Ac-RA 11.2 ± 7.1, Co-RA: 9 ± 5.7, control 5.9 ± 2.1) and plasma cells (Ac-RA 5.2 ± 2.5, Co-RA 6.9 ± 3.7, control 2.8 ± 1.7) as compared to controls, all p < 0.05. RA patients (controlled and active disease) had higher plasma levels of TNF, IL-2, IL-4, IL-6 and IL-10 than controls (all p < 0.002). RA patients had higher BDNF levels (Ac-RA 17,354.4 ± 5357.3, Co-RA 13,841.2 ± 5953.7, control 11,543.3 ± 3772), but lower GDNF levels [median (interquartile range) Ac-RA 0 pg/ml (0.0), Co-RA 0 pg/ml (4.6) and control 4.7 pg/ml (18.1)] than controls (all p < 0.05). RA patients had global cognitive impairment, which was associated with disease activity and immune changes.

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Affiliation(s)

Laura E Petersen Laboratory of Stress Immunology, School of Sciences, Pontifical Catholic University of the Rio Grande do Sul (PUCRS), Porto Alegre, Brazil
Talita S A Baptista Developmental Cognitive Neuroscience Laboratory (DCNL), Faculty of Psychology, PUCRS, Porto Alegre, Brazil
Júlia K Molina Developmental Cognitive Neuroscience Laboratory (DCNL), Faculty of Psychology, PUCRS, Porto Alegre, Brazil
Julia G Motta Laboratory of Stress Immunology, School of Sciences, Pontifical Catholic University of the Rio Grande do Sul (PUCRS), Porto Alegre, Brazil
Aline do Prado Division of Rheumatology, São Lucas Hospital, PUCRS, Porto Alegre, Brazil
Deise M Piovesan Division of Rheumatology, São Lucas Hospital, PUCRS, Porto Alegre, Brazil
Tatiana de Nardi Developmental Cognitive Neuroscience Laboratory (DCNL), Faculty of Psychology, PUCRS, Porto Alegre, Brazil
Thiago W Viola Developmental Cognitive Neuroscience Laboratory (DCNL), Faculty of Psychology, PUCRS, Porto Alegre, Brazil
Érica L M Vieira Interdisciplinary Laboratory of Medical Investigation, School of Medicine, Federal University of Minas Gerais (UFMG), Belo Horizonte, Brazil
Antonio L Teixeira Interdisciplinary Laboratory of Medical Investigation, School of Medicine, Federal University of Minas Gerais (UFMG), Belo Horizonte, Brazil.,Neuropsychiatry Program, Department of Psychiatry and Behavioral Sciences, The University of Texas Health Science Center at Houston, Houston, TX, USA
Rodrigo Grassi-Oliveira Laboratory of Stress Immunology, School of Sciences, Pontifical Catholic University of the Rio Grande do Sul (PUCRS), Porto Alegre, Brazil.,Developmental Cognitive Neuroscience Laboratory (DCNL), Faculty of Psychology, PUCRS, Porto Alegre, Brazil
Moisés Evandro Bauer Laboratory of Stress Immunology, School of Sciences, Pontifical Catholic University of the Rio Grande do Sul (PUCRS), Porto Alegre, Brazil. .,National Institute of Science and Technology on Neuroimmunomodulation (INCT-NIM), Rio de Janeiro, Brazil. .,Instituto de Pesquisas Biomédicas, Faculdade de Biociências, Hospital São Lucas da PUCRS, Av. Ipiranga 6690, 2° andar, P.O. Box 1429, Porto Alegre, RS, 90610-000, Brazil.

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Meade T, Manolios N, Cumming SR, Conaghan PG, Katz P. Cognitive Impairment in Rheumatoid Arthritis: A Systematic Review. Arthritis Care Res (Hoboken) 2017;70:39-52. [DOI: 10.1002/acr.23243] [Citation(s) in RCA: 66] [Impact Index Per Article: 8.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/29/2016] [Accepted: 03/21/2017] [Indexed: 01/08/2023]

Georgopoulos AP, James LM, Carpenter AF, Engdahl BE, Leuthold AC, Lewis SM. Gulf War illness (GWI) as a neuroimmune disease. Exp Brain Res 2017;235:3217-3225. [PMID: 28762055 DOI: 10.1007/s00221-017-5050-0] [Citation(s) in RCA: 39] [Impact Index Per Article: 4.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/11/2017] [Accepted: 07/26/2017] [Indexed: 01/21/2023]

Abstract

Gulf War illness (GWI) is a chronic disease characterized by the involvement of several organs, including the brain (Christova et al., Exp Brain Res doi: 10.1007/s00221-017-5010-8 , 2017). In a previous study (Georgopoulos et al., J Neural Eng 4:349-355, 2015), we identified six protective alleles from Class II human leukocyte antigen (HLA) genes, and more recently, we investigated the brain correlates of this protection (James et al., EBioMedicine 13:72-79, 2016). Those and other studies (Israeli, Lupus, 21:190-194, 2012) suggested an involvement of the immune system in GWI. In a recent study (Engdahl et al., EBioMedicine doi: 10.1016/j.ebiom.2016.08.030 , 2016), we showed that the brain pattern of synchronous neural interactions (SNI; Georgopoulos et al., J Neural Eng 4:349-355, 2007) in GWI is distinctly different from that in healthy controls. Here we focused on the SNI itself, as a basic measure of neural communication (irrespective of specific connections) and compared it between GWI and seven other diseases that cover a broad spectrum of etiology and pathophysiology. Specifically, we sought to determine which, if any, of those diseases might resemble GWI SNI, overall and within the HLA protective domain, and thus gain further knowledge regarding the nature of GWI brain abnormality. We studied a total of 962 participants from a healthy control population (N = 583) and eight different diseases, including GWI (N = 40), schizophrenia (SZ; N = 21), Alzheimer's disease (AD; N = 66), posttraumatic stress disorder (PTSD; N = 159), major depressive disorder (MDD; N = 10), relapsing-remitting multiple sclerosis (RRMS; N = 43), Sjögren's syndrome (SS; N = 32), and rheumatoid arthritis (RA; N = 8). They all underwent a resting-state magnetoencephalographic (MEG) scan to calculate SNIs. Data were analyzed using analysis of covariance (ANCOVA) with disease as fixed factor, and sex and age as covariates. We found that GWI SNIs differed significantly from control SZ, AD, PTSD and MDD but not from RRMS, SS and RA. In addition, we compared GWI to RRMS, SS and RA with respect to SNIs of MEG sensor pairs that were related to the HLA alleles protective for GWI (James et al., EBioMedicine 13:72-79, 2016). We found that GWI SNIs did not differ significantly from any of these three diseases but they did so from control SZ, AD, PTSD and MDD. These findings indicate that (a) GWI brain synchronicity does not differ significantly from that of known immune-related diseases (RRMS, SS, RA), and (b) that this SNI similarity is present within the HLA-related SNIs. In contrast, GWI SNIs differed significantly from those of the other diseases. We conclude that altered brain communication in GWI likely reflects immune-related processes, as postulated previously (James et al., EBioMedicine 13:72-79, 2016). By extension, these findings also indicate that functional brain abnormalities in RRMS, SS and RA might be, in part, due to lack of protective HLA alleles as documented for GWI (Georgopoulos et al., EBioMedicine 3:79-85, 2015).

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Affiliation(s)

Apostolos P Georgopoulos Brain Sciences Center (11B), Minneapolis Veterans Affairs Health Care System, One Veterans Drive, Minneapolis, MN, 55417, USA. .,Department of Neuroscience, University of Minnesota Medical School, Minneapolis, MN, 55455, USA. .,Center for Cognitive Sciences, University of Minnesota, Minneapolis, MN, 55455, USA. .,Department of Psychiatry, University of Minnesota Medical School, Minneapolis, MN, 55455, USA. .,Department of Neurology, University of Minnesota Medical School, Minneapolis, MN, 55455, USA.
Lisa M James Brain Sciences Center (11B), Minneapolis Veterans Affairs Health Care System, One Veterans Drive, Minneapolis, MN, 55417, USA.,Department of Neuroscience, University of Minnesota Medical School, Minneapolis, MN, 55455, USA.,Center for Cognitive Sciences, University of Minnesota, Minneapolis, MN, 55455, USA.,Department of Psychiatry, University of Minnesota Medical School, Minneapolis, MN, 55455, USA
Adam F Carpenter Brain Sciences Center (11B), Minneapolis Veterans Affairs Health Care System, One Veterans Drive, Minneapolis, MN, 55417, USA.,Department of Neurology, University of Minnesota Medical School, Minneapolis, MN, 55455, USA
Brian E Engdahl Brain Sciences Center (11B), Minneapolis Veterans Affairs Health Care System, One Veterans Drive, Minneapolis, MN, 55417, USA.,Department of Neuroscience, University of Minnesota Medical School, Minneapolis, MN, 55455, USA.,Center for Cognitive Sciences, University of Minnesota, Minneapolis, MN, 55455, USA.,Department of Psychology, University of Minnesota, Minneapolis, USA
Arthur C Leuthold Brain Sciences Center (11B), Minneapolis Veterans Affairs Health Care System, One Veterans Drive, Minneapolis, MN, 55417, USA.,Department of Neuroscience, University of Minnesota Medical School, Minneapolis, MN, 55455, USA
Scott M Lewis Brain Sciences Center (11B), Minneapolis Veterans Affairs Health Care System, One Veterans Drive, Minneapolis, MN, 55417, USA.,Department of Neurology, University of Minnesota Medical School, Minneapolis, MN, 55455, USA

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Autoantibodies against myelin sheath and S100β are associated with cognitive dysfunction in patients with rheumatoid arthritis. Clin Rheumatol 2017;36:1959-1968. [PMID: 28656478 DOI: 10.1007/s10067-017-3724-4] [Citation(s) in RCA: 23] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/11/2017] [Revised: 05/18/2017] [Accepted: 06/04/2017] [Indexed: 11/08/2022]

Abstract

Rheumatoid arthritis (RA) has been associated with cognitive impairment and peripheral production of autoantibodies. Autoantibodies against central nervous system (CNS) proteins and S100 calcium-binding β (S100β) were found increased in diseases characterized by cognitive impairment like Alzheimer disease and Neuropsychiatric Systemic Lupus Erythematosus (NPSLE). The aim of this study was to investigate the plasma levels of autoantibodies against myelin basic protein (anti-MBP), myelin oligodendrocyte glycoprotein (anti-MOG) and S100β, and their relationships with cognitive performance in RA patients. Twenty patients with active rheumatoid arthritis and 19 age-, sex-, and schooling-matched healthy controls were recruited. Multiple dimensions of cognitive function were evaluated by structured clinical questionnaires. Autoantibodies and S100β levels were assessed by ELISAs. Patients had significantly higher levels of anti-MBP IgG (17.51 ± 1.36 vs. 5.24 ± 0.53 ng/mL), anti-MOG IgG (5.68 ± 1.34 vs. 0.51 ± 0.49 ng/mL), and S100β protein (2.24 ± 0.50 vs. 0.47 ± 0.06) than controls (all p < 0.0001). After adjusting for potential confounders, RA group presented worse cognitive performance involving the working memory and executive functions such as inhibition, flexibility, and mental control in parallel to higher autoantibodies and S100β levels than healthy controls (all p < 0.001). Levels of anti-MBP were negatively associated with delayed verbal recall (DVR; r = -0.42, p = 0.005), Stroop Color-Word (r = -0.48, p = 0.004), and N-Back Total scores (r = -0.59, p < 0.0001) and positively with Trail Making Test B (TMB, r = 0.53, p = 0.001). Negative correlation was found between levels of anti-MOG and DVR (r = -0.64, p < 0.0001), N-Back Total scores (r = -0.35, p = 0.03), Stroop Color-Word (r = -0.51, p = 0.001), and positively with TMB (r = 0.50, p = 0.003). S100β levels were associated with DVR (r = -0.51, p = 0.002), TMB (r = 0.46, p = 0.008), Stroop Color-Word (r = -0.67, p < 0.0001), and N-Back Total (r = -0.52, p = 0.003). RA is associated with impaired cognitive performance associated with higher levels of CNS-related autoantibodies and S100β levels. Given the importance of myelin integrity to cognition, our data indicate that these autoantibodies may be harmful to proper cognitive function.

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Alam J, Jantan I, Bukhari SNA. Rheumatoid arthritis: Recent advances on its etiology, role of cytokines and pharmacotherapy. Biomed Pharmacother 2017;92:615-633. [PMID: 28582758 DOI: 10.1016/j.biopha.2017.05.055] [Citation(s) in RCA: 188] [Impact Index Per Article: 23.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/11/2017] [Revised: 05/01/2017] [Accepted: 05/10/2017] [Indexed: 01/13/2023] Open

Abstract

An autoimmune disease is defined as a clinical syndrome resulted from an instigation of both T cell and B cell or individually, in the absence of any present infection or any sort of distinguishable cause. Clonal deletion of auto reactive cells remains the central canon of immunology for decades, keeping the role of T cell and B cell aside, which are actually the guards to recognize the entry of foreign body. According to NIH, 23.5 million Americans are all together affected by these diseases. They are rare, but with the exception of RA. Rheumatoid arthritis is chronic and systemic autoimmune response to the multiple joints with unknown ethology, progressive disability, systemic complications, early death and high socioeconomic costs. Its ancient disease with an old history found in North American tribes since 1500 BCE, but its etiology is yet to be explored. Current conventional and biological therapies used for RA are not fulfilling the need of the patients but give only partial responses. There is a lack of consistent and liable biomarkers of prognosis therapeutic response, and toxicity. Rheumatoid arthritis is characterized by hyperplasic synovium, production of cytokines, chemokines, autoantibodies like rheumatoid factor (RF) and anticitrullinated protein antibody (ACPA), osteoclastogensis, angiogenesis and systemic consequences like cardiovascular, pulmonary, psychological, and skeletal disorders. Cytokines, a diverse group of polypeptides, play critical role in the pathogenesis of RA. Their involvement in autoimmune diseases is a rapidly growing area of biological and clinical research. Among the proinflammatory cytokines, IL-1α/β and TNF-α trigger the intracellular molecular signalling pathway responsible for the pathogenesis of RA that leads to the activation of mesenchymal cell, recruitment of innate and adaptive immune system cells, activation of synoviocytes which in term activates various mediators including tumour necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), interleukin-6 (IL-6) and interleukin-8 (IL-8), resulting in inflamed synovium, increase angiogenesis and decrease lymphangiogensis. Their current pharmacotherapy should focus on their three phases of progression i.e. prearthritis phase, transition phase and clinical phase. In this way we will be able to find a way to keep the balance between the pro and anti-inflammatory cytokines that is believe to be the dogma of pathogenesis of RA. For this we need to explore new agents, whether from synthetic or natural source to find the answers for unresolved etiology of autoimmune diseases and to provide a quality of life to the patients suffering from these diseases specifically RA.

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Nataf S. Evolution, immunity and the emergence of brain superautoantigens. F1000Res 2017;6:171. [PMID: 28529699 PMCID: PMC5419255 DOI: 10.12688/f1000research.10950.1] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Accepted: 02/16/2017] [Indexed: 12/20/2022] Open

Abstract

While some autoimmune disorders remain extremely rare, others largely predominate the epidemiology of human autoimmunity. Notably, these include psoriasis, diabetes, vitiligo, thyroiditis, rheumatoid arthritis and multiple sclerosis. Thus, despite the quasi-infinite number of "self" antigens that could theoretically trigger autoimmune responses, only a limited set of antigens, referred here as superautoantigens, induce pathogenic adaptive responses. Several lines of evidence reviewed in this paper indicate that, irrespective of the targeted organ (e.g. thyroid, pancreas, joints, brain or skin), a significant proportion of superautoantigens are highly expressed in the synaptic compartment of the central nervous system (CNS). Such an observation applies notably for GAD65, AchR, ribonucleoproteins, heat shock proteins, collagen IV, laminin, tyrosine hydroxylase and the acetylcholinesterase domain of thyroglobulin. It is also argued that cognitive alterations have been described in a number of autoimmune disorders, including psoriasis, rheumatoid arthritis, lupus, Crohn's disease and autoimmune thyroiditis. Finally, the present paper points out that a great majority of the "incidental" autoimmune conditions notably triggered by neoplasms, vaccinations or microbial infections are targeting the synaptic or myelin compartments. On this basis, the concept of an immunological homunculus, proposed by Irun Cohen more than 25 years ago, is extended here in a model where physiological autoimmunity against brain superautoantigens confers both: i) a crucial evolutionary-determined advantage via cognition-promoting autoimmunity; and ii) a major evolutionary-determined vulnerability, leading to the emergence of autoimmune disorders in Homo sapiens. Moreover, in this theoretical framework, the so called co-development/co-evolution model, both the development (at the scale of an individual) and evolution (at the scale of species) of the antibody and T-cell repertoires are coupled to those of the neural repertoires (i.e. the distinct neuronal populations and synaptic circuits supporting cognitive and sensorimotor functions). Clinical implications and future experimental insights are also presented and discussed.

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van Erp S, Ercan E, Breedveld P, Brakenhoff L, Ghariq E, Schmid S, Osch MV, van Buchem M, Emmer B, van der Grond J, Wolterbeek R, Hommes D, Fidder H, van der Wee N, Huizinga T, van der Heijde D, Middelkoop H, Ronen I, van der Meulen-de Jong A. Cerebral magnetic resonance imaging in quiescent Crohn’s disease patients with fatigue. World J Gastroenterol 2017;23:1018-1029. [PMID: 28246475 PMCID: PMC5311090 DOI: 10.3748/wjg.v23.i6.1018] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/26/2016] [Revised: 11/14/2016] [Accepted: 12/08/2016] [Indexed: 02/06/2023] Open

Cognitive dysfunction correlates with elevated serum S100B concentration in drug-free acutely relapsed patients with schizophrenia. Psychiatry Res 2017;247:6-11. [PMID: 27863321 DOI: 10.1016/j.psychres.2016.09.029] [Citation(s) in RCA: 20] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/03/2016] [Revised: 09/04/2016] [Accepted: 09/20/2016] [Indexed: 02/07/2023]

Tomasevic-Todorovic S, Boskovic K, Filipovic D, Milekic B, Grajic M, Hanna F. Auditory Event-Related P300 Potentials in Rheumatoid Arthritis Patients. NEUROPHYSIOLOGY+ 2015. [DOI: 10.1007/s11062-015-9510-5] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/08/2022]

Hamed SA. Variant of multiple sclerosis with dementia and tumefactive demyelinating brain lesions. World J Clin Cases 2015;3:525-532. [PMID: 26090374 PMCID: PMC4468900 DOI: 10.12998/wjcc.v3.i6.525] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/16/2014] [Revised: 12/26/2014] [Accepted: 03/18/2015] [Indexed: 02/05/2023] Open

Rathbone ATL, Tharmaradinam S, Jiang S, Rathbone MP, Kumbhare DA. A review of the neuro- and systemic inflammatory responses in post concussion symptoms: Introduction of the "post-inflammatory brain syndrome" PIBS. Brain Behav Immun 2015;46:1-16. [PMID: 25736063 DOI: 10.1016/j.bbi.2015.02.009] [Citation(s) in RCA: 59] [Impact Index Per Article: 5.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/10/2014] [Revised: 02/08/2015] [Accepted: 02/09/2015] [Indexed: 12/22/2022] Open

Abstract

Post-concussion syndrome is an aggregate of symptoms that commonly present together after head injury. These symptoms, depending on definition, include headaches, dizziness, neuropsychiatric symptoms, and cognitive impairment. However, these symptoms are common, occurring frequently in non-head injured controls, leading some to question the existence of post-concussion syndrome as a unique syndrome. Therefore, some have attempted to explain post-concussion symptoms as post-traumatic stress disorder, as they share many similar symptoms and post-traumatic stress disorder does not require head injury. This explanation falls short as patients with post-concussion syndrome do not necessarily experience many key symptoms of post-traumatic stress disorder. Therefore, other explanations must be sought to explain the prevalence of post-concussion like symptoms in non-head injury patients. Many of the situations in which post-concussion syndrome like symptoms may be experienced such as infection and post-surgery are associated with systemic inflammatory responses, and even neuroinflammation. Post-concussion syndrome itself has a significant neuroinflammatory component. In this review we examine the evidence of neuroinflammation in post-concussion syndrome and the potential role systemic inflammation plays in post-concussion syndrome like symptoms. We conclude that given the overlap between these conditions and the role of inflammation in their etiologies, a new term, post-inflammatory brain syndromes (PIBS), is necessary to describe the common outcomes of many different inflammatory insults. The concept of post-concussion syndrome is in its evolution therefore, the new term post-inflammatory brain syndromes provides a better understanding of etiology of its wide-array of symptoms and the wide array of conditions they can be seen in.

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Selim ZI, Hamed SA, Elattar AM. Peripheral and central auditory pathways function with rheumatoid arthritis. INTERNATIONAL JOURNAL OF CLINICAL RHEUMATOLOGY 2015. [PMID: 21695659 DOI: 10.2217/ijr.15.7] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/21/2022]

Fuggle NR, Howe FA, Allen RL, Sofat N. New insights into the impact of neuro-inflammation in rheumatoid arthritis. Front Neurosci 2014;8:357. [PMID: 25414636 PMCID: PMC4222329 DOI: 10.3389/fnins.2014.00357] [Citation(s) in RCA: 42] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/01/2014] [Accepted: 10/17/2014] [Indexed: 12/28/2022] Open

Cutolo M, Kitas GD, van Riel PLCM. Burden of disease in treated rheumatoid arthritis patients: going beyond the joint. Semin Arthritis Rheum 2013;43:479-88. [PMID: 24080116 DOI: 10.1016/j.semarthrit.2013.08.004] [Citation(s) in RCA: 84] [Impact Index Per Article: 7.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/24/2013] [Revised: 08/12/2013] [Accepted: 08/13/2013] [Indexed: 12/11/2022]

von Bauer R, Oikonomou D, Sulaj A, Mohammed S, Hotz-Wagenblatt A, Gröne HJ, Arnold B, Falk C, Luethje D, Erhardt A, Stern DM, Bierhaus A, Nawroth PP. CD166/ALCAM mediates proinflammatory effects of S100B in delayed type hypersensitivity. THE JOURNAL OF IMMUNOLOGY 2013;191:369-77. [PMID: 23729438 DOI: 10.4049/jimmunol.1201864] [Citation(s) in RCA: 29] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]

Current World Literature. Curr Opin Rheumatol 2013;25:398-409. [DOI: 10.1097/bor.0b013e3283604218] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/25/2022]

Different coexpressions of arthritis-relevant genes between different body organs and different brain regions in the normal mouse population. Gene X 2013;515:396-402. [DOI: 10.1016/j.gene.2012.12.054] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/25/2012] [Accepted: 12/03/2012] [Indexed: 11/21/2022] Open

Abda EA, Selim ZI, Radwan MEM, Mahmoud NM, Herdan OM, Mohamad KA, Hamed SA. Markers of acute neuropsychiatric systemic lupus erythematosus: a multidisciplinary evaluation. Rheumatol Int 2012;33:1243-53. [PMID: 23064543 DOI: 10.1007/s00296-012-2531-0] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/01/2011] [Accepted: 09/23/2012] [Indexed: 11/08/2022]