Environmental risk factors in multiple sclerosis.

Expert Rev Neurother

University Lecturer, Eulerweg 4, D-64347 Griesheim, Germany.

Published: March 2010

The etiology of multiple sclerosis is, at present, not definitely known, but genetic and environmental factors play a role in its causation. Environmental causes have a predominant impact. Epidemiologic research has contributed considerably to the identification of external risk factors in this multifactorial setting, but methodological constraints still play a major part. Viral and other microbial agents have drawn much attention, although none of them is a necessary condition for the disease. This is true also for the Epstein-Barr virus, for which most data, including prospective data, supports a role in the majority of multiple sclerosis patients. In parallel, the hypothesis is still attractive in that it is not the virus per se, but rather more the age when it infects the human being that is the crucial matter. Other risk factors, such as tobacco smoking and vitamin D deficiency, which have immunomodulating properties, may also play some role, although the latter is not compatible with all data of the descriptive epidmiology of multiple sclerosis. Diet might be of considerable importance, all the more since multiple sclerosis can be ecologically attributed to a certain food patterns and is inversely associated with others (e.g., the 'Mediterranean diet'). The hypothesis that the preservation of meat by nitrite and wood smoke plays a role, and the protective influence of a fish and, possibly, a vegetable diet, are supported by some studies, but methodological constraints limit, at present, definite conclusions. A new avenue is the search for an interaction between genetic and environmental causes, and also between several environmental factors that might lead to new approaches for prevention and, perhaps, for the treatment of multiple sclerosis.

Download full-text PDF

Source
http://dx.doi.org/10.1586/ern.10.7DOI Listing

Publication Analysis

Top Keywords

multiple sclerosis
24
risk factors
12
genetic environmental
8
environmental factors
8
play role
8
methodological constraints
8
multiple
6
sclerosis
6
environmental
5
factors
5

Similar Publications

The most common genetic cause of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) is an intronic GC repeat expansion in C9orf72. The repeats undergo bidirectional transcription to produce sense and antisense repeat RNA species, which are translated into dipeptide repeat proteins (DPRs). As toxicity has been associated with both sense and antisense repeat-derived RNA and DPRs, targeting both strands may provide the most effective therapeutic strategy.

View Article and Find Full Text PDF

We present a case of a woman in her 40s with disseminated enterovirus infection in the setting of maintenance therapy with ocrelizumab for relapsing-remitting multiple sclerosis. The patient originally presented with fever, bilateral lower limb swelling and hypoalbuminaemia. She subsequently developed a productive cough and diarrhoea, and a viral respiratory multiplex panel detected rhino/enterovirus.

View Article and Find Full Text PDF

A 50-year data-driven model of disability and lesion load trajectories in progressive multiple sclerosis.

Brain Commun

December 2024

UCL Hawkes Institute and UCL Queen Square Institute of Neurology, University College London, London, UK.

This scientific commentary refers to 'A data-driven model of disability progression in progressive multiple sclerosis', by Garbarino . (https://doi.org/10.

View Article and Find Full Text PDF

This study applies the Gaussian process progression model, a Bayesian data-driven disease progression model, to analyse the evolution of primary progressive multiple sclerosis. Utilizing data from 1521 primary progressive multiple sclerosis participants collected within the International Progressive Multiple Sclerosis Alliance Project, the analysis includes 18 581 longitudinal time-points (average follow-up time: 28.2 months) of disability assessments including the expanded disability status scale, symbol digit modalities, timed 25-foot-walk, 9-hole-peg test and of MRI metrics such as T1 and T2 lesion volume and normalized brain volume.

View Article and Find Full Text PDF

Introduction: Although the HaCaT keratinocyte model has been used in previous research to study the effects of antipsoriatic agents, there is still a lack of comprehensive understanding of the mechanism of imiquimod (IMQ)-induced proliferation and signal transduction in psoriasis-like keratinocytes.

Objectives: This study aimed to investigate the molecular mechanisms and pathways associated with psoriasis-like inflammation caused by IMQ in human keratinocytes.

Materials And Methods: HaCaT cells were exposed to different concentrations of IMQ to induce inflammation similar to that observed in psoriasis.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!