Sclerosis, MultipleNEUROKINASENCT04674163
Expression Profile of ERK5 and PKM2 Kinases in Neuroinflammatory Diseases.
A study testing Blood sample and Cerebrospinal fluid (CSF) collection. in people with Sclerosis, Multiple and Guillain-Barre Syndrome, run by Centre Hospitalier Régional d'Orléans.
Trial summary
Demyelinating diseases represent a broad spectrum of disorders and are induced by excessive inflammation most often triggered by an autoimmune mechanism. Some of these pathologies are chronic and affect the central nervous system such as multiple sclerosis (MS), others are monophasic and target the peripheral nervous… Read more about this study
- Who is it for?
- Ages 18 to 80 years
- Conditions the study is for
- Sclerosis, Multiple, Guillain-Barre Syndrome, Inflammation
- What is being tested?
- Blood sample and Cerebrospinal fluid (CSF) collection.
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 0 participants
- Where
- No sites listed yet
- Study dates
- Jan 2023to Jan 2023
- Phase
- Interventional
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 80 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- Man and Woman
- 18 to 80 years old
- Clinical signs that suggest MS or GBS within a month of onset symptom
Who cannot join
- Patient treated with immunosuppressive therapy, immunomodulator, or corticosteroids in chronic treatment
- Patient treated with corticosteroids in the past month
- without social security
- HIV positive serology
- dementia
- pregnant or breastfeeding woman
Show all 9Show fewer
- previous participation in the study
- under judicial protection
- non-cooperating patient
About this study
Official title: NEUROKINASE : Expression Profile of ERK5 and PKM2 Kinases in Neuroinflammatory Diseases.
Demyelinating diseases represent a broad spectrum of disorders and are induced by excessive inflammation most often triggered by an autoimmune mechanism. Some of these pathologies are chronic and affect the central nervous system such as multiple sclerosis (MS), others are monophasic and target the peripheral nervous system such as Guillain Barré syndrome (GBS).
In neuroinflammatory pathologies, the excessive response of the pro-inflammatory Th1 and Th17 lymphocyte lines and the insufficient response of regulatory T lymphocytes (Treg) cause excessive inflammation which is deleterious to the nervous tissue. The regulation of these signaling pathways involves key proteins such as kinases. Modulation of these kinases which could allow the development of new pharmacological targets for neuroinflammation.
Read more
Recent work (unpublished data) has shown an association between the expression of ERK5 and PMK2 kinases, and the clinical severity of experimental allergic encephalomyelitis, a mouse model that mimics multiple sclerosis.
In order to search for new biomarkers and improve our knowledge of the actors of the initial inflammatory phase of neuroinflammatory pathologies, we propose to study the differences in expression of ERK5 and PKM2 kinases in the blood and cerebral spinal fluid (CSF) of patients followed for relapsing-remitting MS and GBS by both RT-qPCR and protein quantification. We also want to study other biological parameters which include characterization of the pro / anti-inflammatory balance by cytokine assay and lymphocyte phenotyping, metabolome study, and mild form neurofilament (NfL) assay.
Read the detailed description
The study of the expression of ERK5 and PKM2 kinases in patients followed for RR MS or GBS, at the beginning of the pathology, will be evaluate.
The usual diagnostic workup for MS and GBS will be performed in order to classify patients into 4 groups :
- Group 1 : control group. Patients that do not fulfill the criteria for MS or GBS and in whom no differential diagnosis was made.
Subgroups 1a and 1b will be formed by respective pairing with groups 2 and 3.
- Group 2 : patients with RR MS confirmed by Macdonald criteria (2017)
- Group 3 : patients with GBS confirmed by the association of the usual clinical and electrophysiological signs.
- Group 4 : patients in whom a differential diagnosis has been identified to explain the symptoms. These patients will be excluded from the analysis.
An additional blood sample (25 mL) and cerebrospinal fluid (CSF) sample (2mL) will be taken from all patients in order to study the laboratory parameters of this study. Peripheral blood mononuclear cells (PBMCs) and neutrophils will be isolated from the blood using a Percoll gradient. Group 4 samples will not be analyzed.
The analysis will focus on the comparison of laboratory parameters between group 2 and 3, between group 1a and 2, and between 1b and 3.
- / Expression of ERK5 and PKM2 kinases The investigators wish to analyze the expression of ERK5 and PKM2 by RT-qPCR to investigate the transcriptome on RNA level and by Western Blot and ELISA to investigate the phosphorylated and total forms of the two kinases. RT-qPCR require RNA extraction, reverse transcription into cDNA and then amplification of the genes encoding ERK5 and PKM2 using specific primers designed beforehand. The results will be compared with those obtained with primers of the HPRT gene.
- / Study of the balance between pro and anti-inflammatory action The investigators wish to characterize the balance of pro and anti-inflammatory activity by studying lymphocyte phenotyping and determining the level of cytokines. Lymphocyte phenotyping will be performed by flow cytometry from PBMCs. The populations studied will include the Th1, Th2, Th9, Th17, Th22, Treg and TFH populations. The panel of mainly inflammatory cytokines will be studied in plasma and in CSF by ELISA. The panel includes the following cytokines: IL17, TNF, IL6, Il 1β, IL 10, IL33, IL12, IL 23
- / Metabolome analysis The databases on human metabolomes include more than 40,000 metabolites and allow the establishment of metabolic profiles in different pathological contexts by supervised and unsupervised statistical analysis techniques. Metabolome analyzes will be performed from plasma and CSF. These analyzes will be carried out by liquid chromatography coupled with mass spectrometry (LC-MS) by the Metabohub network (MetaboHUB-Clermont for plasma analyzes and MetaboHUB-Saclay for CSF analyzes).
- / Measure of the neurofilament light chain (NfL)
There is growing interest in neurofilament's measure in the blood and in particular in the CSF. High levels of neurofilaments are evidence of neuronal loss, regardless of the initial mechanism. Neurofilament light chain (NfL) seems to be the most relevant form to measure axonal loss. In MS, increased NfL was observed during the first two months of acute relapse. Conversely, there are few data on the kinetics of NfL's levels in peripheral demyelinating diseases.
The investigators intend to study NfL levels in blood and CSF to determine if there is an increase in NfL levels in patients followed for GBS and to compare NfL levels of these patients (group 3) with patients followed for MS (group 2).
- Conditions
- Sclerosis, Multiple, Guillain-Barre Syndrome, Inflammation
- Being tested
- Blood sample and Cerebrospinal fluid (CSF) collection.
- Keywords
- ERK5 kinase, M2 Type Pyruvate Kinase, cytokines
- Medical subject headings
- Multiple Sclerosis, Guillain-Barre Syndrome, Inflammation
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Blood sample and Cerebrospinal fluid (CSF) collection.Biological
An additional blood sample (25 ml) and a cerebrospinal fluid (CSF) sample (2 ml) will be taken.
| Study group | Role | What they receive |
|---|---|---|
| Patients with clinical signs that suggest Multiple Sclerosis (MS) or Guillain Barré Syndrome (GBS) | Experimental | Not described Receives: Biological: Blood sample and Cerebrospinal fluid (CSF) collection. |
What is being measured
The primary outcome is the main question the study is designed to answer.
Expression of genes encoding ERK5 and PKM2 kinases by RT-qPCR
The expression of ERK5 and PKM2 by RT-qPCR will be analyze to investigate the transcriptome on RNA level.
RT-qPCR require RNA extraction, reverse transcription into cDNA and then amplification of the genes encoding ERK5 and PKM2 using specific primers designed beforehand. The results will be compared with those obtained with primers of the HPRT gene.
These analyzes are carried out using lymphocytes and neutrophils isolated from the blood sample.
Measured: Day 0
Secondary outcomes (4)
Lymphocyte phenotyping
Lymphocyte phenotyping will be performed by flow cytometry from PBMCs. We will use antibodies against Th1, Th2, Th9, Th17, Th22, Treg and TFH populations.
Measured: Day 0
Cytokine levels
A panel of cytokines, mainly pro-inflammatory, will be studied in plasma and in CSF by ELISA. The panel includes the following cytokines: IL17, TNF, IL6, Il 1β, IL 10, IL33, IL12, IL 23
Measured: Day 0
Metabolome analysis
Metabolome analyzes will be performed from plasma and CSF. These analyzes will be carried out by liquid chromatography coupled with mass spectrometry (LC-MS) by the Metabohub network (MetaboHUB-Clermont for plasma analyzes and MetaboHUB-Saclay for CSF analyzes).
Measured: Day 0
Measure of the neurofilament light chain (NfL)
NfL levels in blood and CSF will be studied to determine if there is an increase in NfL levels in patients followed for GBS and to compare the NfL levels of these patients with patients followed for MS.
Measured: Day 0
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted19 Dec 2020
- Study startJan 2023 (estimated)
- Primary completionJan 2023 (estimated)
- Study completionJan 2023 (estimated)
Why it stopped: no practitioner
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (8)Papers the sponsor has linked to this study.
- Other trials for Sclerosis, MultipleStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Other
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Enrolment
- 0 participants (actual)
Sponsor and investigators
- Lead sponsor
- Centre Hospitalier Régional d'Orléans
- Sponsor type
- University, hospital or other
- Collaborators
- Immunologie et Neurogénétique Expérimentales et Moléculaires (INEM)
- Responsible party
- Sponsor
- Investigators
- Pascal AUZOU, Dr, Principal investigator, CHR Orléans
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT04674163
- Sponsor's protocol ID
- CHRO-2018-07
- Acronym
- NEUROKINASE
- Status last verified
- Jan 2023
- First submitted
- 14 Dec 2020
- Last updated
- 23 Jan 2023
- Results posted
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
Gaetani L, Salvadori N, Lisetti V, Eusebi P, Mancini A, Gentili L, Borrelli A, Portaccio E, Sarchielli P, Blennow K, Zetterberg H, Parnetti L, Calabresi P, Di Filippo M. Cerebrospinal fluid neurofilament light chain tracks cognitive impairment in multiple sclerosis. J Neurol. 2019 Sep;266(9):2157-2163. doi: 10.1007/s00415-019-09398-7. Epub 2019 May 25.
PubMed 31129709Kamil K, Yazid MD, Idrus RBH, Das S, Kumar J. Peripheral Demyelinating Diseases: From Biology to Translational Medicine. Front Neurol. 2019 Mar 19;10:87. doi: 10.3389/fneur.2019.00087. eCollection 2019.
PubMed 30941082Khalil M, Teunissen CE, Otto M, Piehl F, Sormani MP, Gattringer T, Barro C, Kappos L, Comabella M, Fazekas F, Petzold A, Blennow K, Zetterberg H, Kuhle J. Neurofilaments as biomarkers in neurological disorders. Nat Rev Neurol. 2018 Oct;14(10):577-589. doi: 10.1038/s41582-018-0058-z.
PubMed 30171200Kuhle J, Plattner K, Bestwick JP, Lindberg RL, Ramagopalan SV, Norgren N, Nissim A, Malaspina A, Leppert D, Giovannoni G, Kappos L. A comparative study of CSF neurofilament light and heavy chain protein in MS. Mult Scler. 2013 Oct;19(12):1597-603. doi: 10.1177/1352458513482374. Epub 2013 Mar 25.
PubMed 23529999Rostami A, Ciric B. Role of Th17 cells in the pathogenesis of CNS inflammatory demyelination. J Neurol Sci. 2013 Oct 15;333(1-2):76-87. doi: 10.1016/j.jns.2013.03.002. Epub 2013 Apr 8.
PubMed 23578791Thompson AJ, Banwell BL, Barkhof F, Carroll WM, Coetzee T, Comi G, Correale J, Fazekas F, Filippi M, Freedman MS, Fujihara K, Galetta SL, Hartung HP, Kappos L, Lublin FD, Marrie RA, Miller AE, Miller DH, Montalban X, Mowry EM, Sorensen PS, Tintore M, Traboulsee AL, Trojano M, Uitdehaag BMJ, Vukusic S, Waubant E, Weinshenker BG, Reingold SC, Cohen JA. Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria. Lancet Neurol. 2018 Feb;17(2):162-173. doi: 10.1016/S1474-4422(17)30470-2. Epub 2017 Dec 21.
PubMed 29275977Venken K, Hellings N, Thewissen M, Somers V, Hensen K, Rummens JL, Medaer R, Hupperts R, Stinissen P. Compromised CD4+ CD25(high) regulatory T-cell function in patients with relapsing-remitting multiple sclerosis is correlated with a reduced frequency of FOXP3-positive cells and reduced FOXP3 expression at the single-cell level. Immunology. 2008 Jan;123(1):79-89. doi: 10.1111/j.1365-2567.2007.02690.x. Epub 2007 Sep 25.
PubMed 17897326Yuan A, Rao MV, Veeranna, Nixon RA. Neurofilaments and Neurofilament Proteins in Health and Disease. Cold Spring Harb Perspect Biol. 2017 Apr 3;9(4):a018309. doi: 10.1101/cshperspect.a018309.
PubMed 28373358
Study at a glance
From the registry record, last updated by the sponsor on 23 Jan 2023. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- NEUROKINASE : Expression Profile of ERK5 and PKM2 Kinases in Neuroinflammatory Diseases.
- ClinicalTrials.gov ID
- NCT04674163
- Acronym / sponsor ID
- NEUROKINASE / CHRO-2018-07
- Conditions
- Sclerosis, Multiple, Guillain-Barre Syndrome, Inflammation
- Keywords
- ERK5 kinase, M2 Type Pyruvate Kinase, cytokines
- Study type
- Interventional
- Recruitment status
- WithdrawnReason stopped: no practitioner
- Enrolment
- 0 participants (actual)
- Lead sponsor
- Centre Hospitalier Régional d'OrléansUniversity, hospital or other
- Collaborators
- Immunologie et Neurogénétique Expérimentales et Moléculaires (INEM)
- Study start
- Jan 2023 (estimated)
- Primary completion
- Jan 2023 (estimated)
- Study completion
- Jan 2023 (estimated)
- First posted
- 19 Dec 2020 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Demyelinating diseases represent a broad spectrum of disorders and are induced by excessive inflammation most often triggered by an autoimmune mechanism. Some of these pathologies are chronic and affect the central nervous system such as multiple sclerosis (MS), others are monophasic and target the peripheral nervous system such as Guillain Barré syndrome (GBS).
In neuroinflammatory pathologies, the excessive response of the pro-inflammatory Th1 and Th17 lymphocyte lines and the insufficient response of regulatory T lymphocytes (Treg) cause excessive inflammation which is deleterious to the nervous tissue. The regulation of these signaling pathways involves key proteins such as kinases. Modulation of these kinases which could allow the development of new pharmacological targets for neuroinflammation.
Recent work (unpublished data) has shown an association between the expression of ERK5 and PMK2 kinases, and the clinical severity of experimental allergic encephalomyelitis, a mouse model that mimics multiple sclerosis.
In order to search for new biomarkers and improve our knowledge of the actors of the initial inflammatory phase of neuroinflammatory pathologies, we propose to study the differences in expression of ERK5 and PKM2 kinases in the blood and cerebral spinal fluid (CSF) of patients followed for relapsing-remitting MS and GBS by both RT-qPCR and protein quantification. We also want to study other biological parameters which include characterization of the pro / anti-inflammatory balance by cytokine assay and lymphocyte phenotyping, metabolome study, and mild form neurofilament (NfL) assay.
Detailed description
The study of the expression of ERK5 and PKM2 kinases in patients followed for RR MS or GBS, at the beginning of the pathology, will be evaluate.
The usual diagnostic workup for MS and GBS will be performed in order to classify patients into 4 groups :
- Group 1 : control group. Patients that do not fulfill the criteria for MS or GBS and in whom no differential diagnosis was made.
Subgroups 1a and 1b will be formed by respective pairing with groups 2 and 3.
- Group 2 : patients with RR MS confirmed by Macdonald criteria (2017)
- Group 3 : patients with GBS confirmed by the association of the usual clinical and electrophysiological signs.
- Group 4 : patients in whom a differential diagnosis has been identified to explain the symptoms. These patients will be excluded from the analysis.
An additional blood sample (25 mL) and cerebrospinal fluid (CSF) sample (2mL) will be taken from all patients in order to study the laboratory parameters of this study. Peripheral blood mononuclear cells (PBMCs) and neutrophils will be isolated from the blood using a Percoll gradient. Group 4 samples will not be analyzed.
The analysis will focus on the comparison of laboratory parameters between group 2 and 3, between group 1a and 2, and between 1b and 3.
- / Expression of ERK5 and PKM2 kinases The investigators wish to analyze the expression of ERK5 and PKM2 by RT-qPCR to investigate the transcriptome on RNA level and by Western Blot and ELISA to investigate the phosphorylated and total forms of the two kinases. RT-qPCR require RNA extraction, reverse transcription into cDNA and then amplification of the genes encoding ERK5 and PKM2 using specific primers designed beforehand. The results will be compared with those obtained with primers of the HPRT gene.
- / Study of the balance between pro and anti-inflammatory action The investigators wish to characterize the balance of pro and anti-inflammatory activity by studying lymphocyte phenotyping and determining the level of cytokines. Lymphocyte phenotyping will be performed by flow cytometry from PBMCs. The populations studied will include the Th1, Th2, Th9, Th17, Th22, Treg and TFH populations. The panel of mainly inflammatory cytokines will be studied in plasma and in CSF by ELISA. The panel includes the following cytokines: IL17, TNF, IL6, Il 1β, IL 10, IL33, IL12, IL 23
- / Metabolome analysis The databases on human metabolomes include more than 40,000 metabolites and allow the establishment of metabolic profiles in different pathological contexts by supervised and unsupervised statistical analysis techniques. Metabolome analyzes will be performed from plasma and CSF. These analyzes will be carried out by liquid chromatography coupled with mass spectrometry (LC-MS) by the Metabohub network (MetaboHUB-Clermont for plasma analyzes and MetaboHUB-Saclay for CSF analyzes).
- / Measure of the neurofilament light chain (NfL)
There is growing interest in neurofilament's measure in the blood and in particular in the CSF. High levels of neurofilaments are evidence of neuronal loss, regardless of the initial mechanism. Neurofilament light chain (NfL) seems to be the most relevant form to measure axonal loss. In MS, increased NfL was observed during the first two months of acute relapse. Conversely, there are few data on the kinetics of NfL's levels in peripheral demyelinating diseases.
The investigators intend to study NfL levels in blood and CSF to determine if there is an increase in NfL levels in patients followed for GBS and to compare NfL levels of these patients (group 3) with patients followed for MS (group 2).
Study design
- Primary purpose
- Other
- Allocation
- Not applicable
- Intervention model
- Single group
- Masking
- None (open label)
- Number of arms
- 1
| Arm | Type | Receives |
|---|---|---|
| Patients with clinical signs that suggest Multiple Sclerosis (MS) or Guillain Barré Syndrome (GBS) | Experimental | Biological: Blood sample and Cerebrospinal fluid (CSF) collection. |
Who may qualify
- Ages
- 18 to 80 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (3 listed)
- Man and Woman
- 18 to 80 years old
- Clinical signs that suggest MS or GBS within a month of onset symptom
Key exclusion criteria (9 listed)
- Patient treated with immunosuppressive therapy, immunomodulator, or corticosteroids in chronic treatment
- Patient treated with corticosteroids in the past month
- without social security
- HIV positive serology
- dementia
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Blood sample and Cerebrospinal fluid (CSF) collection.An additional blood sample (25 ml) and a cerebrospinal fluid (CSF) sample (2 ml) will be taken. | Biological | Patients with clinical signs that suggest Multiple Sclerosis (MS) or Guillain Barré Syndrome (GBS) |
Primary outcome
Expression of genes encoding ERK5 and PKM2 kinases by RT-qPCR
Time frame: Day 0
The expression of ERK5 and PKM2 by RT-qPCR will be analyze to investigate the transcriptome on RNA level. RT-qPCR require RNA extraction, reverse transcription into cDNA and then amplification of the genes encoding ERK5 and PKM2 using specific primers designed beforehand. The results will be compared with those obtained with primers of the HPRT gene. These analyzes are carried out using lymphocytes and neutrophils isolated from the blood sample.
4 secondary outcomes
Lymphocyte phenotyping
Time frame: Day 0
Cytokine levels
Time frame: Day 0
Metabolome analysis
Time frame: Day 0
Measure of the neurofilament light chain (NfL)
Time frame: Day 0
Results and safety
The study was withdrawn before enrolling participants, so there are no results.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 23 Jan 2023.
- Background: PubMed 31129709Gaetani L, Salvadori N, Lisetti V, Eusebi P, Mancini A, Gentili L, Borrelli A, Portaccio E, Sarchielli P, Blennow K, Zetterberg H, Parnetti L, Calabresi P, Di Filippo M. Cerebrospinal fluid neurofilament light chain tracks cognitive impairment in multiple sclerosis. J Neurol. 2019 Sep;266(9):2157-2163. doi: 10.1007/s00415-019-09398-7. Epub 2019 May 25.
- Background: PubMed 30941082Kamil K, Yazid MD, Idrus RBH, Das S, Kumar J. Peripheral Demyelinating Diseases: From Biology to Translational Medicine. Front Neurol. 2019 Mar 19;10:87. doi: 10.3389/fneur.2019.00087. eCollection 2019.
- Background: PubMed 30171200Khalil M, Teunissen CE, Otto M, Piehl F, Sormani MP, Gattringer T, Barro C, Kappos L, Comabella M, Fazekas F, Petzold A, Blennow K, Zetterberg H, Kuhle J. Neurofilaments as biomarkers in neurological disorders. Nat Rev Neurol. 2018 Oct;14(10):577-589. doi: 10.1038/s41582-018-0058-z.
- Background: PubMed 23529999Kuhle J, Plattner K, Bestwick JP, Lindberg RL, Ramagopalan SV, Norgren N, Nissim A, Malaspina A, Leppert D, Giovannoni G, Kappos L. A comparative study of CSF neurofilament light and heavy chain protein in MS. Mult Scler. 2013 Oct;19(12):1597-603. doi: 10.1177/1352458513482374. Epub 2013 Mar 25.
- Background: PubMed 23578791Rostami A, Ciric B. Role of Th17 cells in the pathogenesis of CNS inflammatory demyelination. J Neurol Sci. 2013 Oct 15;333(1-2):76-87. doi: 10.1016/j.jns.2013.03.002. Epub 2013 Apr 8.
- Background: PubMed 29275977Thompson AJ, Banwell BL, Barkhof F, Carroll WM, Coetzee T, Comi G, Correale J, Fazekas F, Filippi M, Freedman MS, Fujihara K, Galetta SL, Hartung HP, Kappos L, Lublin FD, Marrie RA, Miller AE, Miller DH, Montalban X, Mowry EM, Sorensen PS, Tintore M, Traboulsee AL, Trojano M, Uitdehaag BMJ, Vukusic S, Waubant E, Weinshenker BG, Reingold SC, Cohen JA. Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria. Lancet Neurol. 2018 Feb;17(2):162-173. doi: 10.1016/S1474-4422(17)30470-2. Epub 2017 Dec 21.
- Background: PubMed 17897326Venken K, Hellings N, Thewissen M, Somers V, Hensen K, Rummens JL, Medaer R, Hupperts R, Stinissen P. Compromised CD4+ CD25(high) regulatory T-cell function in patients with relapsing-remitting multiple sclerosis is correlated with a reduced frequency of FOXP3-positive cells and reduced FOXP3 expression at the single-cell level. Immunology. 2008 Jan;123(1):79-89. doi: 10.1111/j.1365-2567.2007.02690.x. Epub 2007 Sep 25.
- Background: PubMed 28373358Yuan A, Rao MV, Veeranna, Nixon RA. Neurofilaments and Neurofilament Proteins in Health and Disease. Cold Spring Harb Perspect Biol. 2017 Apr 3;9(4):a018309. doi: 10.1101/cshperspect.a018309.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Pascal AUZOU, Dr principal investigator
CHR Orléans
Questions about this trial
What is this clinical trial studying?
A study testing Blood sample and Cerebrospinal fluid (CSF) collection. in people with Sclerosis, Multiple and Guillain-Barre Syndrome, run by Centre Hospitalier Régional d'Orléans.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 3 inclusion and 9 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: withdrawn, as of the sponsor's last update on 23 Jan 2023. Status can change between updates, so confirm with the study contact before making plans.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study was withdrawn before enrolling participants, so there are no results.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Expression of genes encoding ERK5 and PKM2 kinases by RT-qPCR (time frame: Day 0). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT04674163, which also lists 8 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 23 Jan 2023.