Publications by authors named "Guy Laureys"

19 Publications

  • Page 1 of 1

A clinician's perspective on yellow fever vaccine-associated neurotropic disease.

J Travel Med 2020 11;27(7)

Department of Clinical Sciences, Institute of Tropical Medicine, Kronenburgstraat 43, 2000 Antwerp, Belgium.

Yellow fever (YF) causes high fever, liver dysfunction, renal failure, hypercoagulopathy and platelet dysfunction and can lead to shock and death with a case-fatality ratio of 20-50%. YF vaccination results in long-lasting protective immunity. Serious adverse events (SAEs), such as YF vaccine-associated neurotropic disease (YEL-AND) are rare. We present a case of a 56-year-old Caucasian man with fever, headache, cognitive problems at the emergency department. He received a primary YF vaccination 4 weeks prior to symptom onset. Cerebrospinal fluid tested positive (POS) for YF virus by reverse transcriptase polymerase chain reaction and confirmed diagnosis of YEL-AND. The patient recovered with symptomatic treatment. We reviewed published clinical reports on YEL-AND indexed for MEDLINE. We identified and analyzed 53 case reports. Forty-five patients were male and eight were female. Twenty-nine cases met criteria for definite YEL-AND and twenty-four for suspected YEL-AND according to YF Vaccine Safety Working Group. We applied the Brighton Collaboration diagnostic criteria to assess the diagnostic accuracy of the clinical diagnoses and found meningoencephalitis in 38 reported YEL-AND cases, Guillain Barré Syndrome (GBS) in seven, Acute Disseminated Encephalomyelitis (ADEM) in six and myelitis in five. Thirty-five patients recovered or improved; however, not all cases had a complete follow-up. The prognosis of YEL-AND presenting with GBS, ADEM or myelitis was poor. Fourteen patients received therapy (corticosteroids, intravenous immunoglobulins and/or plasmapheresis). In conclusion, YF vaccine-associated neurotropic disease is a very rare but SAE after YF vaccination. We described a case of YEL-AND and propose a standardized clinical workup of this condition based on a review of the literature. Centralized registration of complications of YF vaccination is encouraged.
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http://dx.doi.org/10.1093/jtm/taaa172DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7649383PMC
November 2020

Deciphering the Morphology of Motor Evoked Potentials.

Front Neuroinform 2020 14;14:28. Epub 2020 Jul 14.

I-Biostat, Data Science Institute, Hasselt University, Diepenbeek, Belgium.

Motor Evoked Potentials (MEPs) are used to monitor disability progression in multiple sclerosis (MS). Their morphology plays an important role in this process. Currently, however, there is no clear definition of what constitutes a normal or abnormal morphology. To address this, five experts independently labeled the morphology (normal or abnormal) of the same set of 1,000 MEPs. The intra- and inter-rater agreement between the experts indicates they agree on the concept of morphology, but differ in their choice of threshold between normal and abnormal morphology. We subsequently performed an automated extraction of 5,943 time series features from the MEPs to identify a valid proxy for morphology, based on the provided labels. To do this, we compared the cross-validation performances of one-dimensional logistic regression models fitted to each of the features individually. We find that the approximate entropy (ApEn) feature can accurately reproduce the majority-vote labels. The performance of this feature is evaluated on an independent test set by comparing to the majority vote of the neurologists, obtaining an AUC score of 0.92. The model slightly outperforms the average neurologist at reproducing the neurologists consensus-vote labels. We can conclude that MEP morphology can be consistently defined by pooling the interpretations from multiple neurologists and that ApEn is a valid continuous score for this. Having an objective and reproducible MEP morphological abnormality score will allow researchers to include this feature in their models, without manual annotation becoming a bottleneck. This is crucial for large-scale, multi-center datasets. An exploratory analysis on a large single-center dataset shows that ApEn is potentially clinically useful. Introducing an automated, objective, and reproducible definition of morphology could help overcome some of the barriers that are currently obstructing broad adoption of evoked potentials in daily care and patient follow-up, such as standardization of measurements between different centers, and formulating guidelines for clinical use.
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http://dx.doi.org/10.3389/fninf.2020.00028DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7381179PMC
July 2020

End of dose interval symptoms in patients treated with natalizumab: A role for serum cytokines?

Mult Scler Relat Disord 2020 Jun 22;41:102020. Epub 2020 Feb 22.

Department of Neurology, UZ Gent, Corneel Heymanslaan 10, Gent, Belgium. Electronic address:

Background: Many natalizumab treated patients experience end of dose interval (EDI) symptoms towards the end of the administration cycle. Natalizumab has previously shown to influence cytokine profiles in relapsing remitting MS patients. We hypothesize that EDI symptoms might be explained by variability in serum cytokine levels during natalizumab treatment.

Methods: 42 relapsing remitting MS patients were included. Participants were evaluated before natalizumab administration (day 0) and 7 days afterwards (day 7). At both time points fatigue, depressed mood and cognition were evaluated using the fatigue severity scale (FSS), the visual analogue scale for fatigue (VAS-F), the symbol digit modality test (SDMT) and the inventory for depressive symptomatology (IDS-SR). Serum samples were tested for concentrations of IL-6, IFN-γ and TNF-α at both timepoints. On day 7 an additional EDI questionnaire was completed. Data were analyzed with SPSS by means of non-parametric tests.

Results: EDI symptoms were reported by 59.5%. Although fatigue was most frequently reported, fatigue scales did not significantly change from day 0 to 7 in (fatigued) EDI patients. Mood and cognition significantly ameliorated in both EDI and non-EDI patients. Cytokines remained stable at day 0 vs 7 except for a significant increase in IFN-γ. On day 0, IFN-γ concentration was positively correlated with a depressed mood in the whole cohort, and with mood and fatigue in the EDI group. Depressed mood positively whilst cognition negatively correlated with IFN-γ concentration on day 0 in the EDI subgroup reporting fatigue. No significant correlations between IL-6 nor TNF-α and symptom scores could be found.

Conclusion: In our study EDI symptoms could not be objectified since EDI and non-EDI groups did not differ in terms of change in mood, cognition and fatigue between day 0 and 7 suggesting that symptom recrudescence could be a subjective experience. Although our results need to be interpreted cautiously, we found no clear correlation between studied serum cytokines concentrations and the occurrence of EDI symptoms.
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http://dx.doi.org/10.1016/j.msard.2020.102020DOI Listing
June 2020

Clinical and therapeutic predictors of disease outcomes in AQP4-IgG+ neuromyelitis optica spectrum disorder.

Mult Scler Relat Disord 2020 Feb 25;38:101868. Epub 2019 Nov 25.

CORe, Department of Medicine, University of Melbourne, Melbourne, Australia; Department of Neurology, Royal Melbourne Hospital, Melbourne, Australia; Department of Neurology, Royal Melbourne Hospital, Melbourne, Australia. Electronic address:

Background: Aquaporin-4-IgG positive (AQP4-IgG+) Neuromyelitis Optica Spectrum Disorder (NMOSD) is an uncommon central nervous system autoimmune disorder. Disease outcomes in AQP4-IgG+NMOSD are typically measured by relapse rate and disability. Using the MSBase, a multi-centre international registry, we aimed to examine the impact immunosuppressive therapies and patient characteristics as predictors of disease outcome measures in AQP4-IgG+NMOSD.

Method: This MSBase cohort study of AQP4-IgG+NMOSD patients examined modifiers of relapse in a multivariable proportional hazards model and expanded disability status score (EDSS) using a mixed effects model.

Results: 206 AQP4-IgG+ patients were included (median follow-up 3.7 years). Age (hazard ratio [HR] = 0.82 per decade, p = 0.001), brainstem onset (HR = 0.45, p = 0.009), azathioprine (HR = 0.46, p<0.001) and mycophenolate mofetil (HR = 0.09, p = 0.012) were associated with a reduced risk of relapse. A greater EDSS was associated with age (β = 0.45 (per decade), p<0.001) and disease duration (β = 0.07 per year, p<0.001). A slower increase in EDSS was associated with azathioprine (β = -0.48, p<0.001), mycophenolate mofetil (β = -0.69, p = 0.04) and rituximab (β = -0.35, p = 0.024).

Interpretation: This study has demonstrated that azathioprine and mycophenolate mofetil reduce the risk of relapses and disability progression is modified by azathioprine, mycophenolate mofetil and rituximab. Age and disease duration were the only patient characteristics that modified the risk of relapse and disability in our cohort.
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http://dx.doi.org/10.1016/j.msard.2019.101868DOI Listing
February 2020

Redefining the Multiple Sclerosis Severity Score (MSSS): The effect of sex and onset phenotype.

Mult Scler 2020 11 31;26(13):1765-1774. Epub 2019 Oct 31.

Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia.

Background: The Multiple Sclerosis Severity Score (MSSS) is a widely used measure of the disability progression rate. However, the global MSSS may not be the best basis for comparison between all patient groups.

Objective: We evaluated sex-specific and onset phenotype-specific MSSS matrices to determine if they were more effective than the global MSSS as a basis for comparison within these subsets.

Methods: Using a large international dataset of multiple sclerosis (MS) patient records and the original MSSS algorithm, we constructed global, sex-specific and onset phenotype-specific MSSS matrices. We compared matrices using permutation analysis.

Results: Our final dataset included 30,203 MS cases, with 28.9% males and 6.5% progressive-onset cases. Our global MSSS matrix did not differ from previously published data ( > 0.05). The progressive-onset-specific matrix differed significantly from the relapsing-onset-specific matrix ( < 0.001), with lower MSSS attributed to cases with the same Expanded Disability Status Score (EDSS) and disease duration. When evaluated with a simulation, using an onset-specific MSSS improved statistical power in mixed cohorts. There were no significant differences by sex.

Conclusion: The differences in the disability accrual rate between progressive- and relapsing-onset MS have a significant effect on MSSS. An onset-specific MSSS should be used when comparing the rate of disability progression among progressive-onset cases and for mixed cohorts.
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http://dx.doi.org/10.1177/1352458519881994DOI Listing
November 2020

Cladribine in myasthenia gravis: A case urging for prudence.

Muscle Nerve 2019 05 22;59(5):E38. Epub 2019 Feb 22.

Department of Neurology, UZ Gent, Corneel Heymanslaan 10, 9000, Gent, Belgium.

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http://dx.doi.org/10.1002/mus.26446DOI Listing
May 2019

[Indications and follow-up for autologous hematopoietic stem cell transplantation in multiple sclerosis: Guidelines from the Francophone Society of Bone Marrow Transplantation and Cellular Therapy (SFGM-TC) in association with the Francophone Society of Multiple Sclerosis].

Bull Cancer 2019 Jan 5;106(1S):S92-S101. Epub 2018 Dec 5.

Hôpital Saint-Louis, centre de référence des maladies auto-immunes systémiques rares d'Île-de-France, filière FAI2R, IUH EA-3518, UF04, unité de médecine interne, maladies auto-immunes et pathologie vasculaire, 1, avenue Claude-Vellefaux, 75475 Paris, France. Electronic address:

The Francophone Society of Bone Marrow Transplantation and Cellular Therapy (SFGM-TC) organized the 8th allogeneic hematopoietic stem cell transplantation clinical practices harmonization workshop series in September 2017 in Lille, France. In this article we give the indications of autologous stem cell transplantation in multiple sclerosis as well as recommendations regarding post-transplant follow-up of patients under the hospice of the SFGM-TC and the Francophone Society of Multiple Sclerosis.
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http://dx.doi.org/10.1016/j.bulcan.2018.11.002DOI Listing
January 2019

EBV-NMDA double positive encephalitis in an immunocompromised patient.

J Neurol Sci 2019 01 3;396:76-77. Epub 2018 Nov 3.

Department of Neurology, Ghent University Hospital, Belgium. Electronic address:

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http://dx.doi.org/10.1016/j.jns.2018.11.001DOI Listing
January 2019

Targeting phosphocreatine metabolism in relapsing-remitting multiple sclerosis: evaluation with brain MRI, H and P MRS, and clinical and cognitive testing.

J Neurol 2018 Nov 5;265(11):2614-2624. Epub 2018 Sep 5.

Department of Neurology, University Hospital Ghent, Ghent, Belgium.

Background/objectives: Fluoxetine and prucalopride might change phosphocreatine (PCr) levels via the cAMP-PKA pathway, an interesting target in the neurodegenerative mechanisms of MS.

Methods: We conducted a two-center double-blind, placebo-controlled, randomized trial including 48 relapsing-remitting MS patients. Patients were randomized to receive placebo (n = 13), fluoxetine (n = 15), or prucalopride (n = 14) for 6 weeks. Proton (H) and phosphorus (P) magnetic resonance spectroscopy (MRS) as well as volumetric and perfusion MR imaging were performed at weeks 0, 2, and 6. Clinical and cognitive testing were evaluated at weeks 0 and 6.

Results: No significant changes were observed for both P and H MRS indices. We found a significant effect on white matter volume and a trend towards an increase in grey matter and whole brain volume in the fluoxetine group at week 2; however, these effects were not sustained at week 6 for white matter and whole brain volume. Fluoxetine and prucalopride showed a positive effect on 9-HPT, depression, and fatigue scores.

Conclusion: Both fluoxetine and prucalopride had a symptomatic effect on upper limb function, fatigue, and depression, but this should be interpreted with caution. No effect of treatment was found on P and H MRS parameters, suggesting that these molecules do not influence the PCr metabolism.
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http://dx.doi.org/10.1007/s00415-018-9039-9DOI Listing
November 2018

A Belgian consensus protocol for autologous hematopoietic stem cell transplantation in multiple sclerosis.

Acta Neurol Belg 2018 Jun 13;118(2):161-168. Epub 2018 Mar 13.

Department of Hematology, Antwerp University Hospital, Wilrijkstraat 10, 2650, Edegem, Belgium.

Multiple sclerosis is considered to be an immune mediated inflammatory disorder of the central nervous system. It mainly affects young, socioeconomic active patients. Although our armamentarium for this disease has significantly evolved in recent years some patients remain refractory to conventional therapies. In these cases, autologous hematopoietic stem cell transplantation can be considered as a therapeutic option. Decreasing morbidity, mortality, and increasing patient awareness have led to rising inquiry by our patients about this treatment option. With the aim of a standardized protocol and data registration, a Belgian working party on stem cell therapy in multiple sclerosis was established. In this paper, we report the consensus protocol of this working party on autologous hematopoietic stem cell transplantation in multiple sclerosis.
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http://dx.doi.org/10.1007/s13760-018-0905-0DOI Listing
June 2018

β₂-adrenergic agonists modulate TNF-α induced astrocytic inflammatory gene expression and brain inflammatory cell populations.

J Neuroinflammation 2014 Jan 30;11:21. Epub 2014 Jan 30.

Department of Neurology, University Hospital Brussels, Center for Neurosciences, Vrije Universiteit Brussel, Laarbeeklaan 101, 1090 Brussels, Belgium.

Background: The NF-κB signaling pathway orchestrates many of the intricate aspects of neuroinflammation. Astrocytic β₂-adrenergic receptors have emerged as potential regulators in central nervous system inflammation and are potential targets for pharmacological modulation. The aim of this study was to elucidate the crosstalk between astrocytic β₂-adrenergic receptors and the TNF-α induced inflammatory gene program.

Methods: Proinflammatory conditions were generated by the administration of TNF-α. Genes that are susceptible to astrocytic crosstalk between β₂-adrenergic receptors (stimulated by clenbuterol) and TNF-α were identified by qPCR-macroarray-based gene expression analysis in a human 1321 N1 astrocytoma cell line. Transcriptional patterns of the identified genes in vitro were validated by RT-PCR on the 1321 N1 cell line as well as on primary rat astrocytes. In vivo expression patterns were examined by intracerebroventricular administration of clenbuterol and/or TNF-α in rats. To examine the impact on the inflammatory cell content of the brain we performed extensive FACS analysis of rat brain immune cells after intracerebroventricular clenbuterol and/or TNF-α administration.

Results: Parallel transcriptional patterns in vivo and in vitro confirmed the relevance of astrocytic β₂-adrenergic receptors as modulators of brain inflammatory responses. Importantly, we observed pronounced effects of β2-adrenergic receptor agonists and TNF-α on IL-6, CXCL2, CXCL3, VCAM1, and ICAM1 expression, suggesting a role in inflammatory brain cell homeostasis. Extensive FACS-analysis of inflammatory cell content in the brain demonstrated that clenbuterol/TNF-α co-administration skewed the T cell population towards a double negative phenotype and induced a shift in the myeloid brain cell population towards a neutrophilic predominance.

Conclusions: Our results show that astrocytic β₂-adrenergic receptors are potent regulators of astrocytic TNF-α-activated genes in vitro and in vivo, and ultimately modulate the molecular network involved in the homeostasis of inflammatory cells in the central nervous system. Astrocytic β₂-adrenergic receptors and their downstream signaling pathway may serve as potential targets to modulate neuroinflammatory responses.
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http://dx.doi.org/10.1186/1742-2094-11-21DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3942172PMC
January 2014

Fluoxetine in progressive multiple sclerosis (FLUOX-PMS): study protocol for a randomized controlled trial.

Trials 2014 Jan 25;15:37. Epub 2014 Jan 25.

Department of Neurology, University Hospital Brussel, Center for Neurosciences Vrije Universiteit Brussel (VUB) UZ Brussel, Laarbeeklaan 101, 1090 Brussels, Belgium.

Background: Currently available disease-modifying treatments acting by modifying the immune response are ineffective in progressive multiple sclerosis (MS), which is caused by a widespread axonal degeneration. Mechanisms suspected to be involved in this widespread axonal degeneration are reduced axonal energy metabolism, axonal glutamate toxicity, and reduced cerebral blood flow. Fluoxetine might theoretically reduce axonal degeneration in MS because it stimulates energy metabolism through enhancing glycogenolysis, stimulates the production of brain-derived neurotrophic factor, and dilates cerebral arterioles. The current document presents the protocol of a clinical trial to test the hypothesis that fluoxetine slows down the progressive phase of MS.

Methods/design: The FLUOX-PMS trial is a multi-center, randomized, controlled and double-blind clinical study. A total of 120 patients with the diagnosis of either secondary or primary progressive MS will be treated either by fluoxetine (40 mg daily) or placebo for a total period of 108 weeks. The primary endpoint is the time to confirmed disease progression defined as either at least a 20% increase in the timed 25-Foot Walk or at least a 20% increase in the 9-Hole Peg Test. Secondary endpoints include the Hauser ambulation index, cognitive changes, fatigue, magnetic resonance imaging of the brain, and in a small subgroup optical coherence tomography.

Discussion: The FLUOX-PMS trial will gives us information as to whether fluoxetine has neuroprotective effects in patients with progressive MS.

Trial Registration: Eudra-CT: 2011-003775-11.
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http://dx.doi.org/10.1186/1745-6215-15-37DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3931920PMC
January 2014

White-matter astrocytes, axonal energy metabolism, and axonal degeneration in multiple sclerosis.

J Cereb Blood Flow Metab 2012 Mar 4;32(3):413-24. Epub 2012 Jan 4.

Department of Neurology, Center for Neurosciences, Universitair Ziekenhuis Brussel, Vrije Universiteit Brussel, Brussel, Belgium.

In patients with multiple sclerosis (MS), a diffuse axonal degeneration occurring throughout the white matter of the central nervous system causes progressive neurologic disability. The underlying mechanism is unclear. This review describes a number of pathways by which dysfunctional astrocytes in MS might lead to axonal degeneration. White-matter astrocytes in MS show a reduced metabolism of adenosine triphosphate-generating phosphocreatine, which may impair the astrocytic sodium potassium pump and lead to a reduced sodium-dependent glutamate uptake. Astrocytes in MS white matter appear to be deficient in β(2) adrenergic receptors, which are involved in stimulating glycogenolysis and suppressing inducible nitric oxide synthase (NOS2). Glutamate toxicity, reduced astrocytic glycogenolysis leading to reduced lactate and glutamine production, and enhanced nitric oxide (NO) levels may all impair axonal mitochondrial metabolism, leading to axonal degeneration. In addition, glutamate-mediated oligodendrocyte damage and impaired myelination caused by a decreased production of N-acetylaspartate by axonal mitochondria might also contribute to axonal loss. White-matter astrocytes may be considered as a potential target for neuroprotective MS therapies.
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http://dx.doi.org/10.1038/jcbfm.2011.193DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3293127PMC
March 2012

Late onset painful cold-aggravated myotonia: three families with SCN4A L1436P mutation.

Neuromuscul Disord 2011 Aug 12;21(8):590-3. Epub 2011 Jun 12.

Department of Neurology, UZ Brussel, Vrije Universiteit Brussel (VUB), Belgium.

We describe three Belgian families with a L1436P mutation in the SCN4A gene, causing a sodium channel myotonia with an atypical clinical presentation, characterized by late onset painful cold-aggravated myotonia. These families represent a distinct phenotype within the spectrum of sodium channel myotonia.
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http://dx.doi.org/10.1016/j.nmd.2011.05.006DOI Listing
August 2011

Interleukin-6, a mental cytokine.

Brain Res Rev 2011 Jun 14;67(1-2):157-83. Epub 2011 Jan 14.

Laboratory of Eukaryotic Signal Transduction and Gene Expression, University of Ghent, K.L. Ledeganckstraat 35, 9000 Gent, Belgium.

Almost a quarter of a century ago, interleukin-6 (IL-6) was discovered as an inflammatory cytokine involved in B cell differentiation. Today, IL-6 is recognized to be a highly versatile cytokine, with pleiotropic actions not only in immune cells, but also in other cell types, such as cells of the central nervous system (CNS). The first evidence implicating IL-6 in brain-related processes originated from its dysregulated expression in several neurological disorders such as multiple sclerosis, Alzheimer's disease and Parkinson's disease. In addition, IL-6 was shown to be involved in multiple physiological CNS processes such as neuron homeostasis, astrogliogenesis and neuronal differentiation. The molecular mechanisms underlying IL-6 functions in the brain have only recently started to emerge. In this review, an overview of the latest discoveries concerning the actions of IL-6 in the nervous system is provided. The central position of IL-6 in the neuroinflammatory reaction pattern, and more specifically, the role of IL-6 in specific neurodegenerative processes, which accompany Alzheimer's disease, multiple sclerosis and excitotoxicity, are discussed. It is evident that IL-6 has a dichotomic action in the CNS, displaying neurotrophic properties on the one hand, and detrimental actions on the other. This is in agreement with its central role in neuroinflammation, which evolved as a beneficial process, aimed at maintaining tissue homeostasis, but which can become malignant when exaggerated. In this perspective, it is not surprising that 'well-meant' actions of IL-6 are often causing harm instead of leading to recovery.
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http://dx.doi.org/10.1016/j.brainresrev.2011.01.002DOI Listing
June 2011

Astrocytes as potential targets to suppress inflammatory demyelinating lesions in multiple sclerosis.

Neurochem Int 2010 Nov 21;57(4):446-50. Epub 2010 Feb 21.

Department of Neurology, University Hospital Brussel, Vrije Universiteit Brussel, Brussels, Belgium.

A hallmark of multiple sclerosis (MS) is the occurrence of focal inflammatory demyelinating lesions in the central nervous system. The prevailing view that activated anti-myelin T cells inherently mediate these lesions has been challenged after observations that these T cells, which are part of the normal immune repertoire, can also intermittently become activated in healthy people and subjects with other diseases. Astrocytes in the white matter of subjects with MS are deficient in beta(2) adrenergic receptors. Stimulation of beta(2) adrenergic receptors increases cAMP, leading to activation of protein kinase A (PKA). beta(2) adrenergic receptor deficiency will reduce the suppressive action of PKA on coactivator class II transactivator (CIITA), which is a key regulator of interferon gamma-induced major histocompatibility (MHC) class II molecule transcription. The expression of MHC class II may deviate astrocytes to function as facultative antigen presenting cells, which can then initiate the inflammatory cascade. In a proof of concept study in MS subjects it was shown that fluoxetine, which activates PKA in astrocytes, reduced the development of focal inflammatory lesions. If confirmed and extended by additional studies, suppressing the antigen presenting capacity of astrocytes could be a novel therapeutic option for the treatment of MS.
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http://dx.doi.org/10.1016/j.neuint.2010.02.012DOI Listing
November 2010

Astrocytic beta(2)-adrenergic receptors: from physiology to pathology.

Prog Neurobiol 2010 Jul 4;91(3):189-99. Epub 2010 Feb 4.

Department of Pharmaceutical Chemistry and Drug Analysis, Vrije Universiteit Brussel, Belgium.

Evidence accumulates for a key role of the beta(2)-adrenergic receptors in the many homeostatic and neuroprotective functions of astrocytes, including glycogen metabolism, regulation of immune responses, release of neurotrophic factors, and the astrogliosis that occurs in response to neuronal injury. A dysregulation of the astrocytic beta(2)-adrenergic-pathway is suspected to contribute to the physiopathology of a number of prevalent and devastating neurological conditions such as multiple sclerosis, Alzheimer's disease, human immunodeficiency virus encephalitis, stroke and hepatic encephalopathy. In this review we focus on the physiological functions of astrocytic beta(2)-adrenergic receptors, and their possible impact in disease states.
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http://dx.doi.org/10.1016/j.pneurobio.2010.01.011DOI Listing
July 2010

Susac syndrome: a case report and PET imaging findings.

Acta Neurol Belg 2009 Sep;109(3):226-30

Department of Neurology, UZ Brussels, Brussels, Belgium.

We describe the case of a twenty-year-old woman with subacute encephalopathy, who subsequently developed hearing loss and ophtalmopathy. The clinical triad and typical findings on magnetic resonance imaging and cerebrospinal fluid analysis led to the diagnosis of Susac syndrome. Brain positron emission tomography showed abnormalities which are comparable with other types of central nervous system vasculitis, and distinct from those found in multiple sclerosis.
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September 2009