Multiple sclerosis epidemiology in Finland: Regional differences and high incidence

2019 ◽  
Vol 139 (4) ◽  
pp. 353-359 ◽  
Author(s):  
Anna-Leena Pirttisalo ◽  
Merja Soilu-Hänninen ◽  
Jussi O. T. Sipilä

ASN NEURO ◽  
2020 ◽  
Vol 12 ◽  
pp. 175909142097960
Author(s):  
Andrew S. Lapato ◽  
Sarah M. Thompson ◽  
Karen Parra ◽  
Seema K. Tiwari-Woodruff

While seizure disorders are more prevalent among multiple sclerosis (MS) patients than the population overall and prognosticate earlier death & disability, their etiology remains unclear. Translational data indicate perturbed expression of astrocytic molecules contributing to homeostatic neuronal excitability, including water channels (AQP4) and synaptic glutamate transporters (EAAT2), in a mouse model of MS with seizures (MS+S). However, astrocytes in MS+S have not been examined. To assess the translational relevance of astrocyte dysfunction observed in a mouse model of MS+S, demyelinated lesion burden, astrogliosis, and astrocytic biomarkers (AQP4/EAAT2/ connexin-CX43) were evaluated by immunohistochemistry in postmortem hippocampi from MS & MS+S donors. Lesion burden was comparable in MS & MS+S cohorts, but astrogliosis was elevated in MS+S CA1 with a concomitant decrease in EAAT2 signal intensity. AQP4 signal declined in MS+S CA1 & CA3 with a loss of perivascular AQP4 in CA1. CX43 expression was increased in CA3. Together, these data suggest that hippocampal astrocytes from MS+S patients display regional differences in expression of molecules associated with glutamate buffering and water homeostasis that could exacerbate neuronal hyperexcitability. Importantly, mislocalization of CA1 perivascular AQP4 seen in MS+S is analogous to epileptic hippocampi without a history of MS, suggesting convergent pathophysiology. Furthermore, as neuropathology was concentrated in MS+S CA1, future study is warranted to determine the pathophysiology driving regional differences in glial function in the context of seizures during demyelinating disease.



Author(s):  
Ali Forouhari ◽  
Ghazale Taheri ◽  
Salari Mehri ◽  
Moosazadeh Mahmood ◽  
Masoud Etemadifar


2019 ◽  
Vol 266 (7) ◽  
pp. 1789-1795 ◽  
Author(s):  
Lisa Langenbruch ◽  
Julia Krämer ◽  
Sati Güler ◽  
Gabriel Möddel ◽  
Sophia Geßner ◽  
...  


2018 ◽  
Vol 26 ◽  
pp. 242
Author(s):  
S. Eskandarieh ◽  
N. Molazadeh ◽  
A.N. Moghadasi ◽  
A.R. Azimi ◽  
M.A. Sahraiain


2020 ◽  
Vol 142 (3) ◽  
pp. 200-209
Author(s):  
Anna‐Leena Pirttisalo ◽  
Merja Soilu‐Hänninen ◽  
Marja‐Liisa Sumelahti ◽  
Olga Krökki ◽  
Annukka Murtonen ◽  
...  


2019 ◽  
Vol 116 (20) ◽  
pp. 10130-10139 ◽  
Author(s):  
Rhonda R. Voskuhl ◽  
Noriko Itoh ◽  
Alessia Tassoni ◽  
Macy Akiyo Matsukawa ◽  
Emily Ren ◽  
...  

Regional differences in neurons, astrocytes, oligodendrocytes, and microglia exist in the brain during health, and regional differences in the transcriptome may occur for each cell type during neurodegeneration. Multiple sclerosis (MS) is multifocal, and regional differences in the astrocyte transcriptome occur in experimental autoimmune encephalomyelitis (EAE), an MS model. MS and EAE are characterized by inflammation, demyelination, and axonal damage, with minimal remyelination. Here, RNA-sequencing analysis of MS tissues from six brain regions suggested a focus on oligodendrocyte lineage cells (OLCs) in corpus callosum. Olig1-RiboTag mice were used to determine the translatome of OLCs in vivo in corpus callosum during the remyelination phase of a chronic cuprizone model with axonal damage. Cholesterol-synthesis gene pathways dominated as the top up-regulated pathways in OLCs during remyelination. In EAE, remyelination was induced with estrogen receptor-β (ERβ) ligand treatment, and up-regulation of cholesterol-synthesis gene expression was again observed in OLCs. ERβ-ligand treatment in the cuprizone model further increased cholesterol synthesis gene expression and enhanced remyelination. Conditional KOs of ERβ in OLCs demonstrated that increased cholesterol-synthesis gene expression in OLCs was mediated by direct effects in both models. To address this direct effect, ChIP assays showed binding of ERβ to the putative estrogen-response element of a key cholesterol-synthesis gene (Fdps). As fetal OLCs are exposed in utero to high levels of estrogens in maternal blood, we discuss how remyelinating properties of estrogen treatment in adults during injury may recapitulate normal developmental myelination through targeting cholesterol homeostasis in OLCs.



2010 ◽  
Vol 9 (5) ◽  
pp. 520-532 ◽  
Author(s):  
Nils Koch-Henriksen ◽  
Per Soelberg Sørensen


2001 ◽  
Vol 103 (1) ◽  
pp. 20-26 ◽  
Author(s):  
M. Pugliatti ◽  
S. Sotgiu ◽  
G. Solinas ◽  
P. Castiglia ◽  
M. I. Pirastru ◽  
...  


Author(s):  
Andre Guerra

Multiple sclerosis (MS) has long been labeled as a neurological disease with a high incidence among Canadians, women in particular. The disease first manifests itself in young adulthood (between the ages of 15 and 40 years). Areas of demyelination with a proliferation of astrocytes are found scattered in the white matter of MS patients, this leads to muscle weakness, numbness, disequilibrium, sphincter disturbance and other neurological dysfunctions. Recently Dr. Paolo Zamboni, a vascular surgeon at the University of Ferrara in Italy, found that many multiple sclerosis patients have a narrowing of some of the neck veins responsible for draining blood from the brain. According to Dr. Zamboni, this narrowing of the blood vessels leads to the deposit of iron in the defected veins, which restricts blood flow and is responsible for some of the MS complications. Dr. Zamboni achieved unblocking of the veins through angioplasty, a procedure normally used to open arteries affected by atherosclerosis. In one of his trials, 65 patients were given the procedure, which decreased the rate of occurrence of lesions, from 50% to 12% in patients. There was an improvement in mental and physical quality of life in most of the patients in this trial. Ethical questions are also discussed in this review. Dr. Zamboni`s studies suggest a genetic inheritance of factors that may lead to MS. Should health care providers institute a screening procedure in newborns? Would these screenings be mandatory? Would the screenings be free? 



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