Expression analysis of PINK1 and PINK1-AS in multiple sclerosis patients versus healthy subjects

2020 ◽  
pp. 1-9
Author(s):  
Mona Patoughi ◽  
Soudeh Ghafouri-Fard ◽  
Shahram Arsang-Jang ◽  
Mohammad Taheri
Keyword(s):  
Multiple Sclerosis ◽  
Expression Analysis ◽  
Healthy Subjects ◽  
Multiple Sclerosis Patients

scholarly journals Expression analysis of protein inhibitor of activated STAT (PIAS) genes in IFNβ-treated multiple sclerosis patients

2018 ◽  
Vol Volume 11 ◽  
pp. 457-463 ◽  
Author(s):  
Mohammad Taheri ◽  
Ghazaleh Azimi ◽  
Arezou Sayad ◽  
Mehrdokht Mazdeh ◽  
Shahram Arsang-Jang ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Expression Analysis ◽  
Protein Inhibitor ◽  
Multiple Sclerosis Patients

TRAIL gene expression analysis in multiple sclerosis patients

2016 ◽  
Vol 24 (1-2) ◽  
pp. 33-38 ◽  
Author(s):  
Mohammad Taheri ◽  
Shirin Nemati ◽  
Abolfazl Movafagh ◽  
Mohammad Saberi ◽  
Reza Mirfakhraie ◽  
...  
Keyword(s):  
Gene Expression ◽  
Multiple Sclerosis ◽  
Expression Analysis ◽  
Gene Expression Analysis ◽  
Multiple Sclerosis Patients

Improvement of hand dexterity following motor cortex rTMS in multiple sclerosis patients with cerebellar impairment

2008 ◽  
Vol 14 (7) ◽  
pp. 995-998 ◽  
Author(s):  
G Koch ◽  
S Rossi ◽  
C Prosperetti ◽  
C Codecà ◽  
F Monteleone ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Transcranial Magnetic Stimulation ◽  
Motor Cortex ◽  
Healthy Subjects ◽  
Magnetic Stimulation ◽  
Repetitive Transcranial Magnetic Stimulation ◽  
Hand Dexterity ◽  
Time Required ◽  
Multiple Sclerosis Patients ◽  
Cerebellar Symptoms

We tested the effects of 5-Hz repetitive transcranial magnetic stimulation (rTMS) over the motor cortex in multiple sclerosis (MS) subjects with cerebellar symptoms. rTMS improved hand dexterity in cerebellar patients ( n = 8) but not in healthy subjects ( n = 7), as detected by a significant transient reduction of the time required to complete the nine-hole pegboard task. rTMS of the motor cortex may be a useful approach to treat cerebellar impairment in MS patients.

scholarly journals Polymorphism of chemokine receptor gene CCR5 in multiple sclerosis patients and in healthy subjects in the Siberian region

2006 ◽  
Vol 5 (3) ◽  
pp. 98-104
Author(s):  
Yu. Yu. Orlova ◽  
V. M. Alifirova ◽  
N. V. Cherdyntseva ◽  
P. A. Gervas
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Chemokine Receptor ◽  
Healthy Subjects ◽  
Receptor Gene ◽  
Chronic Inflammatory Disease ◽  
Leading Role ◽  
Multiple Sclerosis Patients ◽  
Chemokine Receptor Gene

Multiple sclerosis is chronic inflammatory disease of the central nervous system in the development of which chemokines of the type Tx1 play the leading role. Chemokines and their receptors participate in the development of multiple sclerosis as a result of drawing immune cells into central nervous system. Mutation of CCR5 delta32 decreases functional activity of the appropriate receptor on cellular surface and thus can reduce migration of leucocytes into foci of injury. Aimed at studying the role of mutation in multiple sclerosis, we compared frequency of gene type CCR5 in peripheral mononuclears of 102 multiple sclerosis patients and in 136 healthy subjects. The results obtained allow to conclude that polymorphism of chemokine receptor gene CCR5del32 is not a leading factor in the susceptibility to multiple sclerosis in the studied population.

FTY720 (fingolimod) treatment tips the balance towards less immunogenic antigen-presenting cells in patients with multiple sclerosis

2015 ◽  
Vol 21 (14) ◽  
pp. 1811-1822 ◽  
Author(s):  
Felix Luessi ◽  
Stefan Kraus ◽  
Bettina Trinschek ◽  
Steffen Lerch ◽  
Robert Ploen ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Dendritic Cells ◽  
Healthy Subjects ◽  
Ex Vivo ◽  
Antigen Presenting Cells ◽  
Direct Effects ◽  
Quantitative Analyses ◽  
Ifn Γ ◽  
Multiple Sclerosis Patients ◽  
Antigen Presenting

Objective: We aimed to clarify whether fingolimod has direct effects on antigen-presenting cells in multiple sclerosis patients. Methods: Frequency and phenotype of directly ex vivo dendritic cells and monocytes were analyzed in 43 individuals, including fingolimod-treated and untreated multiple sclerosis patients as well as healthy subjects. These cells were further stimulated with lipopolysaccharide to determine functional effects of fingolimod treatment. Results: Absolute numbers of CD1c+ dendritic cells and monocytes were not significantly reduced in fingolimod-treated patients indicating that fingolimod did not block the migration of antigen-presenting cells to peripheral blood. CD86 was upregulated on CD1c+ dendritic cells and thus their activation was not impaired under fingolimod treatment. Quantitative analyses of gene transcription in cells and protein content in supernatants from ex vivo CD1c+ dendritic cells and monocytes, however, showed lower secretion of TNFα, IL1-β and IL-6 upon lipopolysaccharide-stimulation. These results could be matched with CD4+MOG-specific transgenic T cells exhibiting reduced levels of TNFα and IFN-γ but not IL-4 upon stimulation with murine dendritic cells loaded with MOG, when treated with fingolimod. Conclusions: Our data indicate that fingolimod – apart from trapping lymphocytes in lymph nodes – exerts its disease-modulating activity by rebalancing the immune tolerance networks by modulation of antigen-presenting cells.

scholarly journals Neurophysiological Correlates of Central Fatigue in Healthy Subjects and Multiple Sclerosis Patients before and after Treatment with Amantadine

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Emiliano Santarnecchi ◽  
Simone Rossi ◽  
Sabina Bartalini ◽  
Massimo Cincotta ◽  
Fabio Giovannelli ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Healthy Subjects ◽  
Silent Period ◽  
Central Fatigue ◽  
Intracortical Inhibition ◽  
Functional Changes ◽  
Chronic Therapy ◽  
Before And After ◽  
Abductor Digiti Minimi ◽  
Multiple Sclerosis Patients

In ten healthy subjects and in ten patients suffering from Multiple Sclerosis (MS), we investigated the cortical functional changes induced by a standard fatiguing repetitive tapping task. The Cortical Silent Period (CSP), an intracortical, mainlyGABAB-mediated inhibitory phenomenon, was recorded by two different hand muscles, one acting as prime mover of the fatiguing index-thumb tapping task (First Dorsal Interosseous, FDI) and the other one not involved in the task but sharing largely overlapping central, spinal, and peripheral innervation (Abductor Digiti Minimi, ADM). At baseline, the CSP was shorter in patients than in controls. As fatigue developed, CSP changes involved both the “fatigued” FDI and the “unfatigued” ADM muscles, suggesting a cortical spread of central fatigue mechanisms. Chronic therapy with amantadine annulled differences in CSP duration between controls and patients, possibly through restoration of more physiological levels of intracortical inhibition in the motor cortex. These inhibitory changes correlated with the improvement of fatigue scales. The CSP may represent a suitable marker of neurophysiological mechanisms accounting for central fatigue generation either in controls or in MS patients, involving corticospinal neural pools supplying not only the fatigued muscle but also adjacent muscles sharing an overlapping cortical representation.

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