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Article ; Online: Author response: Clinical Reasoning: A young woman with respiratory failure, hearing loss, and paraplegia.

Ntranos, Achilles

2017 Volume 89, Issue 9, Page(s) 978

MeSH term(s)	Female ; Hearing Loss ; Humans ; Paraplegia ; Respiratory Insufficiency
Language	English
Publishing date	2017-09-01
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000004306
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Article ; Online: The Microbiome-Gut-Behavior Axis: Crosstalk Between the Gut Microbiome and Oligodendrocytes Modulates Behavioral Responses.

Ntranos, Achilles / Casaccia, Patrizia

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics

2017 Volume 15, Issue 1, Page(s) 31–35

Abstract: Environmental and dietary stimuli have always been implicated in brain development and behavioral responses. The gut, being the major portal of communication with the external environment, has recently been brought to the forefront of this interaction ... ...

Abstract	Environmental and dietary stimuli have always been implicated in brain development and behavioral responses. The gut, being the major portal of communication with the external environment, has recently been brought to the forefront of this interaction with the establishment of a gut-brain axis in health and disease. Moreover, recent breakthroughs in germ-free and antibiotic-treated mice have demonstrated the significant impact of the microbiome in modulating behavioral responses in mice and have established a more specific microbiome-gut-behavior axis. One of the mechanisms by which this axis affects social behavior is by regulating myelination at the prefrontal cortex, an important site for complex cognitive behavior planning and decision-making. The prefrontal cortex exhibits late myelination of its axonal projections that could extend into the third decade of life in humans, which make it susceptible to external influences, such as microbial metabolites. Changes in the gut microbiome were shown to alter the composition of the microbial metabolome affecting highly permeable bioactive compounds, such as p-cresol, which could impair oligodendrocyte differentiation. Dysregulated myelination in the prefrontal cortex is then able to affect behavioral responses in mice, shifting them towards social isolation. The reduced social interactions could then limit microbial exchange, which could otherwise pose a threat to the survival of the existing microbial community in the host and, thus, provide an evolutionary advantage to the specific microbial community. In this review, we will analyze the microbiome-gut-behavior axis, describe the interactions between the gut microbiome and oligodendrocytes and highlight their role in the modulation of social behavior.
MeSH term(s)	Animals ; Gastrointestinal Microbiome ; Humans ; Myelin Sheath ; Oligodendroglia/microbiology ; Prefrontal Cortex/microbiology ; Social Behavior
Language	English
Publishing date	2017-12-20
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2316693-9
ISSN	1878-7479 ; 1933-7213
ISSN (online)	1878-7479
ISSN	1933-7213
DOI	10.1007/s13311-017-0597-9
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Article ; Online: Diagnostic Criteria, Classification and Treatment Goals in Multiple Sclerosis: The Chronicles of Time and Space.

Ntranos, Achilles / Lublin, Fred

Current neurology and neuroscience reports

2016 Volume 16, Issue 10, Page(s) 90

Abstract: Multiple sclerosis (MS) is one of the most diverse human diseases. Since its first description by Charcot in the nineteenth century, the diagnostic criteria, clinical course classification, and treatment goals for MS have been constantly revised and ... ...

Abstract	Multiple sclerosis (MS) is one of the most diverse human diseases. Since its first description by Charcot in the nineteenth century, the diagnostic criteria, clinical course classification, and treatment goals for MS have been constantly revised and updated to improve diagnostic accuracy, physician communication, and clinical trial design. These changes have improved the clinical outcomes and quality of life for patients with the disease. Recent technological and research breakthroughs will almost certainly further change how we diagnose, classify, and treat MS in the future. In this review, we summarize the key events in the history of MS, explain the reasoning behind the current criteria for MS diagnosis, classification, and treatment, and provide suggestions for further improvements that will keep enhancing the clinical practice of MS.
MeSH term(s)	Humans ; Multiple Sclerosis/classification ; Multiple Sclerosis/diagnosis ; Multiple Sclerosis/therapy
Language	English
Publishing date	2016-10
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2057363-7
ISSN	1534-6293 ; 1528-4042
ISSN (online)	1534-6293
ISSN	1528-4042
DOI	10.1007/s11910-016-0688-8
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Article ; Online: Bromodomains: Translating the words of lysine acetylation into myelin injury and repair.

Ntranos, Achilles / Casaccia, Patrizia

Neuroscience letters

2016 Volume 625, Page(s) 4–10

Abstract: Bromodomains are evolutionarily highly conserved α-helical structural motifs that recognize and bind acetylated lysine residues. Lysine acetylation is being increasingly recognized as a major posttranslational modification involved in diverse cellular ... ...

Abstract	Bromodomains are evolutionarily highly conserved α-helical structural motifs that recognize and bind acetylated lysine residues. Lysine acetylation is being increasingly recognized as a major posttranslational modification involved in diverse cellular processes and protein interactions and its deregulation has been implicated in the pathophysiology of various human diseases, such as multiple sclerosis and cancer. Bromodomain-containing proteins can have a wide variety of functions, ranging from histone acetyltransferase activity and chromatin remodeling to transcriptional mediation and co-activation. The role of bromodomains in translating a deregulated cell acetylome into disease phenotypes was recently unveiled by the development of small molecule bromodomain inhibitors. This breakthrough discovery highlighted bromodomain-containing proteins as key players of inflammatory pathways responsible for myelin injury and also demonstrated their role in several aspects of myelin repair including oligodendrocyte differentiation and axonal regeneration.
MeSH term(s)	Acetylation ; Animals ; Cytokines/metabolism ; Demyelinating Diseases/immunology ; Demyelinating Diseases/metabolism ; Epigenesis, Genetic ; Histone Acetyltransferases/metabolism ; Humans ; Inflammation Mediators/metabolism ; Lysine/metabolism ; Protein Processing, Post-Translational ; Regeneration
Chemical Substances	Cytokines ; Inflammation Mediators ; Histone Acetyltransferases (EC 2.3.1.48) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2016-06-20
Publishing country	Ireland
Document type	Journal Article ; Review
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2015.10.015
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Article ; Online: Author response: Clinical Reasoning: A young woman with respiratory failure, hearing loss, and paraplegia.

Ntranos, Achilles / Shoirah, Hazem / Dhamoon, Mandip S / Hahn, David / Naidich, Thomas P / Shin, Susan

Neurology

2017 Volume 89, Issue 9, Page(s) 979

MeSH term(s)	Female ; Hearing Loss ; Humans ; Paraplegia ; Respiratory Insufficiency
Language	English
Publishing date	2017-08-24
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000004309
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Article ; Online: Education Research: Resident education through adult learning in neurology: Implementation and impact.

Shoirah, Hazem / Ntranos, Achilles / Brandstadter, Rachel / Liu, Yangbo / Medina, Elisha / Kwan, Jamie / Krieger, Stephen

Neurology

2018 Volume 91, Issue 5, Page(s) 234–238

Abstract: Objective: To enhance residency education by implementing the 6 principles of adult learning theory (ALT) in a large academic neurology residency program.: Methods: We implemented a set of curricular interventions aimed at Resident Education through ... ...

Abstract	Objective: To enhance residency education by implementing the 6 principles of adult learning theory (ALT) in a large academic neurology residency program. Methods: We implemented a set of curricular interventions aimed at Resident Education through Adult Learning in Neurology (REAL Neurology), in a large, academic neurology residency program. Interventions included didactic reform, increasing resident-as-teacher activities, and enhancing residents' interaction. The primary outcome was the change in mean Residency In-service Training Examination (RITE) percentile between the preintervention and postintervention cohorts, adjusting for US Medical Licensing Examination step 1 and 2 score. Other analysis included evaluating the effect of the duration of intervention exposure on outcome and evaluating the intervention effect on the proportion of advanced performers. Results: A total of 134 RITE score reports were evaluated (87 preintervention and 47 postintervention). The mean RITE score percentile postintervention was 11.7 points higher than preintervention (adjusted, longitudinal analysis: fit linear mixed model, Conclusion: This study evaluated the efficacy and feasibility of an ALT-based curricular program in neurology education. The results show robust and sustainable benefit for residents in training without imposing a financial or logistical burden on programs. REAL Neurology could serve as a model for curricular reform in other programs across subspecialties.
MeSH term(s)	Adult ; Clinical Competence ; Cohort Studies ; Humans ; Internship and Residency/methods ; Internship and Residency/trends ; Neurology/education ; Neurology/methods ; Neurology/trends
Language	English
Publishing date	2018-07-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000005914
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Article ; Online: Clinical Reasoning: A young woman with respiratory failure, hearing loss, and paraplegia.

Ntranos, Achilles / Shoirah, Hazem / Dhamoon, Mandip S / Hahn, David / Naidich, Thomas P / Shin, Susan

Neurology

2017 Volume 88, Issue 10, Page(s) e78–e84

MeSH term(s)	Adult ; Analgesics, Opioid/adverse effects ; Analgesics, Opioid/urine ; Female ; Hearing Loss/chemically induced ; Hearing Loss/diagnosis ; Hearing Loss/urine ; Humans ; Hypoxia/chemically induced ; Hypoxia/diagnosis ; Hypoxia/urine ; Oxycodone/adverse effects ; Oxycodone/urine ; Paraplegia/chemically induced ; Paraplegia/diagnosis ; Paraplegia/urine ; Prescription Drug Overuse/adverse effects ; Respiratory Insufficiency/chemically induced ; Respiratory Insufficiency/diagnosis ; Respiratory Insufficiency/urine
Chemical Substances	Analgesics, Opioid ; Oxycodone (CD35PMG570)
Language	English
Publishing date	2017-03-06
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000003684
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Article ; Online: Bacterial neurotoxic metabolites in multiple sclerosis cerebrospinal fluid and plasma.

Ntranos, Achilles / Park, Hye-Jin / Wentling, Maureen / Tolstikov, Vladimir / Amatruda, Mario / Inbar, Benjamin / Kim-Schulze, Seunghee / Frazier, Carol / Button, Judy / Kiebish, Michael A / Lublin, Fred / Edwards, Keith / Casaccia, Patrizia

Brain : a journal of neurology

2021 Volume 145, Issue 2, Page(s) 569–583

Abstract: The identification of intestinal dysbiosis in patients with neurological and psychiatric disorders has highlighted the importance of gut-brain communication, and yet the question regarding the identity of the components responsible for this cross-talk ... ...

Abstract	The identification of intestinal dysbiosis in patients with neurological and psychiatric disorders has highlighted the importance of gut-brain communication, and yet the question regarding the identity of the components responsible for this cross-talk remains open. We previously reported that relapsing remitting multiple sclerosis patients treated with dimethyl fumarate have a prominent depletion of the gut microbiota, thereby suggesting that studying the composition of plasma and CSF samples from these patients may help to identify microbially derived metabolites. We used a functional xenogeneic assay consisting of cultured rat neurons exposed to CSF samples collected from multiple sclerosis patients before and after dimethyl fumarate treatment to assess neurotoxicity and then conducted a metabolomic analysis of plasma and CSF samples to identify metabolites with differential abundance. A weighted correlation network analysis allowed us to identify groups of metabolites, present in plasma and CSF samples, whose abundance correlated with the neurotoxic potential of the CSF. This analysis identified the presence of phenol and indole group metabolites of bacterial origin (e.g. p-cresol sulphate, indoxyl sulphate and N-phenylacetylglutamine) as potentially neurotoxic and decreased by treatment. Chronic exposure of cultured neurons to these metabolites impaired their firing rate and induced axonal damage, independent from mitochondrial dysfunction and oxidative stress, thereby identifying a novel pathway of neurotoxicity. Clinical, radiological and cognitive test metrics were also collected in treated patients at follow-up visits. Improved MRI metrics, disability and cognition were only detected in dimethyl fumarate-treated relapsing remitting multiple sclerosis patients. The levels of the identified metabolites of bacterial origin (p-cresol sulphate, indoxyl sulphate and N-phenylacetylglutamine) were inversely correlated to MRI measurements of cortical volume and directly correlated to the levels of neurofilament light chain, an established biomarker of neurodegeneration. Our data suggest that phenol and indole derivatives from the catabolism of tryptophan and phenylalanine are microbially derived metabolites, which may mediate gut-brain communication and induce neurotoxicity in multiple sclerosis.
MeSH term(s)	Animals ; Biomarkers ; Dimethyl Fumarate/therapeutic use ; Humans ; Indican ; Multiple Sclerosis/drug therapy ; Multiple Sclerosis, Relapsing-Remitting/drug therapy ; Phenol ; Rats
Chemical Substances	Biomarkers ; Phenol (339NCG44TV) ; Dimethyl Fumarate (FO2303MNI2) ; Indican (N187WK1Y1J)
Language	English
Publishing date	2021-12-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awab320
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Article ; Online: Fumarates target the metabolic-epigenetic interplay of brain-homing T cells in multiple sclerosis.

Ntranos, Achilles / Ntranos, Vasilis / Bonnefil, Valentina / Liu, Jia / Kim-Schulze, Seunghee / He, Ye / Zhu, Yunjiao / Brandstadter, Rachel / Watson, Corey T / Sharp, Andrew J / Katz Sand, Ilana / Casaccia, Patrizia

Brain : a journal of neurology

2019 Volume 142, Issue 3, Page(s) 647–661

Abstract: Cell-permeable formulations of metabolites, such as fumaric acid esters, have been used as highly effective immunomodulators in patients with multiple sclerosis and yet their mechanism of action remains elusive. Since fumaric acid esters are metabolites, ...

Abstract	Cell-permeable formulations of metabolites, such as fumaric acid esters, have been used as highly effective immunomodulators in patients with multiple sclerosis and yet their mechanism of action remains elusive. Since fumaric acid esters are metabolites, and cell metabolism is highly intertwined with the epigenetic regulation of gene expression, we investigated whether this metabolic-epigenetic interplay could be leveraged for therapeutic purposes. To this end we recruited 47 treatment-naïve and 35 fumaric acid ester-treated patients with multiple sclerosis, as well as 16 glatiramer acetate-treated patients as a non-metabolite treatment control. Here we identify a significant immunomodulatory effect of fumaric acid esters on the expression of the brain-homing chemokine receptor CCR6 in CD4 and CD8 T cells of patients with multiple sclerosis, which include T helper-17 and T cytotoxic-17 cells. We report differences in DNA methylation of CD4 T cells isolated from untreated and treated patients with multiple sclerosis, using the Illumina EPIC 850K BeadChip. We first demonstrate that Krebs cycle intermediates, such as fumaric acid esters, have a significantly higher impact on epigenome-wide DNA methylation changes in CD4 T cells compared to amino-acid polymers such as glatiramer acetate. We then define a fumaric acid ester treatment-specific hypermethylation effect on microRNA MIR-21, which is critical for the differentiation of T helper-17 cells. This hypermethylation effect was attributed to the subpopulation of T helper-17 cells using a decomposition analysis and was further validated in an independent prospective cohort of seven patients before and after treatment with fumaric acid esters. In vitro treatment of CD4 and CD8 T cells with fumaric acid esters supported a direct and dose-dependent effect on DNA methylation at the MIR-21 promoter. Finally, the upregulation of miR-21 transcripts and CCR6 expression was inhibited if CD4 or CD8 T cells stimulated under T helper-17 or T cytotoxic-17 polarizing conditions were treated with fumaric acid esters in vitro. These data collectively define a direct link between fumaric acid ester treatment and hypermethylation of the MIR-21 locus in both CD4 and CD8 T cells and suggest that the immunomodulatory effect of fumaric acid esters in multiple sclerosis is at least in part due to the epigenetic regulation of the brain-homing CCR6+ CD4 and CD8 T cells.
MeSH term(s)	Adult ; Brain/immunology ; Brain/metabolism ; CD4-Positive T-Lymphocytes/metabolism ; DNA Methylation/genetics ; Epigenesis, Genetic/genetics ; Female ; Fumarates/metabolism ; Fumarates/pharmacology ; Gene Expression Regulation/genetics ; Glatiramer Acetate/therapeutic use ; Humans ; Immunologic Factors/therapeutic use ; Male ; MicroRNAs/metabolism ; Middle Aged ; Multiple Sclerosis/metabolism ; Multiple Sclerosis/physiopathology ; Prospective Studies ; T-Lymphocytes/metabolism ; T-Lymphocytes/physiology
Chemical Substances	Fumarates ; Immunologic Factors ; MicroRNAs ; Glatiramer Acetate (5M691HL4BO)
Language	English
Publishing date	2019-01-29
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awy344
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Article ; Online: Interleukin-3 coordinates glial-peripheral immune crosstalk to incite multiple sclerosis.

Kiss, Máté G / Mindur, John E / Yates, Abi G / Lee, Donghoon / Fullard, John F / Anzai, Atsushi / Poller, Wolfram C / Christie, Kathleen A / Iwamoto, Yoshiko / Roudko, Vladimir / Downey, Jeffrey / Chan, Christopher T / Huynh, Pacific / Janssen, Henrike / Ntranos, Achilles / Hoffmann, Jan D / Jacob, Walter / Goswami, Sukanya / Singh, Sumnima /

Leppert, David / Kuhle, Jens / Kim-Schulze, Seunghee / Nahrendorf, Matthias / Kleinstiver, Benjamin P / Probert, Fay / Roussos, Panos / Swirski, Filip K / McAlpine, Cameron S

Immunity

2023 Volume 56, Issue 7, Page(s) 1502–1514.e8

Abstract: Glial cells and central nervous system (CNS)-infiltrating leukocytes contribute to multiple sclerosis (MS). However, the networks that govern crosstalk among these ontologically distinct populations remain unclear. Here, we show that, in mice and humans, ...

Abstract	Glial cells and central nervous system (CNS)-infiltrating leukocytes contribute to multiple sclerosis (MS). However, the networks that govern crosstalk among these ontologically distinct populations remain unclear. Here, we show that, in mice and humans, CNS-resident astrocytes and infiltrating CD44
MeSH term(s)	Animals ; Humans ; Mice ; Central Nervous System ; Interleukin-3 ; Microglia ; Multiple Sclerosis ; Neuroglia/metabolism
Chemical Substances	Interleukin-3 ; Il3 protein, mouse
Language	English
Publishing date	2023-05-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2023.04.013
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