Role of serum TRAIL level and TRAIL apoptosis gene expression in multiple sclerosis and relation to brain atrophy

2014 ◽  
Vol 21 (9) ◽  
pp. 1606-1611 ◽  
Author(s):  
Mohamed H. Tawdy ◽  
Maged M. Abd el Nasser ◽  
Sanaa S. Abd el Shafy ◽  
Mona A.F. Nada ◽  
Mohamed Nasr I. El Sirafy ◽  
...  
Keyword(s):  
Gene Expression ◽  
Multiple Sclerosis ◽  
Brain Atrophy ◽  
Apoptosis Gene

Role of serum TRAIL level and TRAIL apoptosis gene in multiple sclerosis and their relation with brain atrophy

2013 ◽  
Vol 333 ◽  
pp. e412-e413
Author(s):  
M. Nada ◽  
M. Tawdy ◽  
M. Abd El Nasser ◽  
S. Abd El Shafy ◽  
M.N. El Sirafy ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Brain Atrophy ◽  
Apoptosis Gene

scholarly journals Cognitive disorders in multiple sclerosis: correlation between neuropsychological, neurophysiological and neuroimaging characteristics

2008 ◽  
Vol 7 (5-1) ◽  
pp. 252-259
Author(s):  
N. F. Musina
Keyword(s):  
Magnetic Resonance Imaging ◽  
Multiple Sclerosis ◽  
Cognitive Functions ◽  
Brain Atrophy ◽  
Mini Mental State Examination ◽  
Cognitive Disorders ◽  
Frontal Assessment Battery ◽  
Resonance Imaging ◽  
State Examination

Multiple sclerosis (MS) — autoimmune disease of CNS, characterized by myelin destruction and axonal damage. To study cognitive functions, the authors used the Mini-Mental State Examination (MMSE), the frontal assessment battery, the procedure developed by A.R. Luriya, neurophysiological characteristics. 71 patients were underwent magnetic resonance imaging. The aim of the study was to analyse the parameters of neuropsychological method, cognitive evoked potentials P300 and the role of brain atrophy in MS. The cognitive functions, the activity of the disease and the expression of brain atrophy are bound by the certain way.

The Role of High‐Frequency MRI Monitoring in the Detection of Brain Atrophy in Multiple Sclerosis

2018 ◽  
Vol 28 (3) ◽  
pp. 328-337 ◽  
Author(s):  
Tomas Uher ◽  
Jan Krasensky ◽  
Lukas Sobisek ◽  
Zdenek Seidl ◽  
Niels Bergsland ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Brain Atrophy ◽  
High Frequency

scholarly journals Microglial CX3CR1I249/M280 variant limits neurogenesis and remyelination in cuprizone-induced multiple sclerosis model

2021 ◽  
Author(s):  
Andrew S Mendiola ◽  
Kaira A Church ◽  
Sandra M Cardona ◽  
Difernando Vanegas ◽  
Shannon A Garcia ◽  
...  
Keyword(s):  
Gene Expression ◽  
Multiple Sclerosis ◽  
Expression Analysis ◽  
Gene Networks ◽  
Gene Expression Analysis ◽  
Neurogenic Niche ◽  
Fractalkine Receptor ◽  
Central Nervous System Repair ◽  
Ms Pathogenesis

Microglia have been implicated in multiple sclerosis (MS) pathogenesis. The fractalkine receptor CX3CR1 regulates the activation of pathogenic microglia in models of MS and the human polymorphic CX3CR1I249/M280 (hCX3CR1I249/M280) variant increases MS disease progression. However, the role of hCX3CR1I249/M280 on microglial activation and central nervous system repair and regenerative mechanisms remain unknown. Therefore, using transgenic mice expressing the hCX3CR1I249/M280 variant, we aimed to determine the contribution of defective CX3CR1 signaling to remyelination and neurogenesis in the cuprizone model of focal demyelination. Here, we report that mice expressing hCX3CR1I249/M280 exhibit marked demyelination and microgliosis follow acute cuprizone treatment. Cuprizone-treated CX3CR1-deficient and fractalkine-deficient mice displayed a comparable phenotype. Nanostring gene expression analysis in demyelinated lesions showed that hCX3CR1I249/M280 upregulates genes associated with inflammation, oxidative stress and disease-associated microglia. In addition, gene expression analysis in the subgranular zone (SGZ) of the hippocampus in hCX3CR1I249/M280 mice was associated with a significant downregulation of gene networks linked to neurogenesis following acute demyelination. Confocal microscopy showed that hCX3CR1I249/M280 or loss of CX3CR1 signaling inhibits the generation of progeny from the neurogenic niche, including cells involved in myelin repair. These results provide evidence for the pathogenic capacity of hCX3CR1I249/M280 on microglia dysfunction and therapeutic targeting of CX3CR1 to promote CNS repair in MS.

scholarly journals The role of MR volumetry in brain atrophy assessment in multiple sclerosis: A review of the literature

2019 ◽  
Vol 28 (7) ◽  
pp. 989-999 ◽  
Author(s):  
Ewelina Marciniewicz ◽  
Joanna Bladowska ◽  
Przemysław Podgórski ◽  
Marek Sąsiadek
Keyword(s):  
Multiple Sclerosis ◽  
Brain Atrophy ◽  
Review Of The Literature ◽  
Mr Volumetry

Common genetic variants in the plasminogen activation pathway are not associated with multiple sclerosis

2013 ◽  
Vol 20 (4) ◽  
pp. 489-491 ◽  
Author(s):  
Mathew B Cox ◽  
Nikola A Bowden ◽  
Rodney J Scott ◽  
Jeannette Lechner-Scott
Keyword(s):  
Gene Expression ◽  
Multiple Sclerosis ◽  
Plasminogen Activation ◽  
Common Genetic Variants ◽  
Modifiable Factors ◽  
Peptidase Inhibitor ◽  
Differential Gene ◽  
Activation Cascade ◽  
Metalloproteinase 9

Matrix metalloproteinase 9 (MMP9) is involved in multiple sclerosis (MS) aetiology. Previously, we identified differential gene expression of plasminogen activation cascade genes in MS patients. Based on our gene expression results, we wanted to identify whether polymorphisms in the genes associated with the plasminogen pathway could predict MS risk. We genotyped 1153 trio families, 727 MS cases and 604 healthy controls for 17 polymorphisms in MMP9, plasminogen activator urokinase (PLAU), PLAU receptor (PLAUR) and serpin peptidase inhibitor/clade 2/member B2 (SERPINB2) genes. No associations were found between the 17 polymorphisms and MS. Also, gene expression levels were analysed according to genotype: no associations were observed. In conclusion despite the consistent evidence for the role of MMP9 and the plasminogen activation cascade in MS, we found no associations between genotype nor gene expression. This suggested there are other potentially modifiable factors influencing gene expression in MS.

scholarly journals Imprinted Genes and Multiple Sclerosis: What Do We Know?

2021 ◽  
Vol 22 (3) ◽  
pp. 1346
Author(s):  
Natalia Baulina ◽  
Ivan Kiselev ◽  
Olga Favorova
Keyword(s):  
Gene Expression ◽  
Multiple Sclerosis ◽  
Molecular Mechanisms ◽  
Imprinted Genes ◽  
Factors Affecting ◽  
Phenotypic Differences ◽  
The Central Nervous System ◽  
Parent Of Origin ◽  
Origin Effects

Multiple sclerosis (MS) is a chronic autoimmune neurodegenerative disease of the central nervous system that arises from interplay between non-genetic and genetic risk factors. The epigenetics functions as a link between these factors, affecting gene expression in response to external influence, and therefore should be extensively studied to improve the knowledge of MS molecular mechanisms. Among others, the epigenetic mechanisms underlie the establishment of parent-of-origin effects that appear as phenotypic differences depending on whether the allele was inherited from the mother or father. The most well described manifestation of parent-of-origin effects is genomic imprinting that causes monoallelic gene expression. It becomes more obvious that disturbances in imprinted genes at the least affecting their expression do occur in MS and may be involved in its pathogenesis. In this review we will focus on the potential role of imprinted genes in MS pathogenesis.

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