Background And Objectives: Multiple Sclerosis (MS) epidemiology is on the path of globalization mainly due to changing environmental factors. The prevalence of MS is on the rise in the Middle East and Persian Gulf region. Our observations has led us to hypothesize a heavy MRI lesion load at the onset of disease in a relatively younger native population. We aimed to estimate and characterize the onset disease on MRI using McDonald's criteria while applying its terms of "Dissemination in Space (DIS) and Dissemination in Time (DIT)".
Materials And Methods: Retrospective review of onset MRI studies of 181 Emirati (native) individuals. Basic demographics were captured. Only 47 patients with Clinically Definite MS (CDMS) were included who had onset diagnostic MRI available. Lesion load was quantified using the specific zones of involvement designated for DIS: (1) Periventricular (PVZ) (I), (2) Juxta-cortical (II) (3) Infra-tentorial (III) and, (4) Spinal cord (IV). PVZ was sub-classified and lesions were quantified. A single enhancing lesion was required for DIT.
Results: Average age of onset was about 26 years with female dominance of about 2 : 1. About 50% had all 4 zones and about 85% had at least 3 zones involved at the onset. Involvement of only 1 zone was rare. Dissemination in time (DIT) in brain and/or cord was present in approximately 50%. Each of the 4 zones were involved in at least 70% of cases. PVZ was not spared in any case with at least 3 lesions present in approx. 95% and ≥12 lesions in approx. half of the patients. Spinal cord specifically cervical cord was involved in up to 80% with typical patchy lesions.
Conclusion: Onset disease characterization using MRI in a young Emirati cohort showed a heavy lesion load in the brain and spinal cord at the onset, signifying cumulative disease before presentation. Disseminated disease also facilitated early diagnosis of MS. The findings have significant potential ramifications for local environmental and cultural factors, as well as disease course and disability progression.
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http://dx.doi.org/10.1155/2019/7460213 | DOI Listing |
Neurol Neuroimmunol Neuroinflamm
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Hospices Civils de Lyon, Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation-Hôpital Neurologique Pierre Wertheimer, Bron Cedex.
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Diabetes Care
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Department of Epidemiology and Biostatistics, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
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BioMarin Pharmaceutical Inc., Novato, CA, United States of America.
The GM2 gangliosidoses, Tay-Sachs disease and Sandhoff disease, are devastating neurodegenerative disorders caused by β-hexosaminidase A (HexA) deficiency. In the Sandhoff disease mouse model, rescue potential was severely reduced when HexA was introduced after disease onset. Here, we assess the effect of recombinant HexA and HexD3, a newly engineered mimetic of HexA optimized for the treatment of Tay-Sachs disease and Sandhoff disease.
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Department of Oncology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330006, Jiangxi Province, China.
The combined use of tocilizumab (TCZ) and immune checkpoint inhibitors (ICIs) in cancer treatment is gaining attention, but preclinical studies are lacking. Our study aims to investigate the synergistic anti-tumor effect of TCZ combined with ICIs and its role in treating immune-related adverse events (irAEs). The clinical significance of high interleukin-6 (IL-6) expression in tumor patients was analyzed from the Cancer Genome Atlas (TCGA) database.
View Article and Find Full Text PDFNeurochem Res
January 2025
Department of Neurology, Affiliated Hospital of Zunyi Medical University, Zunyi, China.
Alzheimer's disease (AD) is a central nervous system degenerative disease with a stealthy onset and a progressive course characterized by memory loss, cognitive dysfunction, and abnormal psychological and behavioral symptoms. However, the pathogenesis of AD remains elusive. An increasing number of studies have shown that oligodendrocyte progenitor cells (OPCs) and oligodendroglial lineage cells (OLGs), especially OPCs and mature oligodendrocytes (OLGs), which are derived from OPCs, play important roles in the pathogenesis of AD.
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