Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

Logo MUG-Forschungsportal

Gewählte Publikation:

SHR Neuro Krebs Kardio Lipid

Fazekas, F; Enzinger, C; Ropele, S; Schmidt, H; Schmidt, R; Strasser-Fuchs, S.
The impact of our genes: consequences of the apolipoprotein E polymorphism in Alzheimer disease and multiple sclerosis.
J NEUROL SCI. 2006; 245(1-2): 35-39.
Web of Science PubMed FullText FullText_MUG Google Scholar


Autor/innen der Med Uni Graz:
Enzinger Christian
Fazekas Franz
Fuchs Siegrid
Ropele Stefan
Schmidt Helena
Schmidt Reinhold

Dimensions Citations:

Plum Analytics:
Epidemiological studies provide strong evidence that susceptibility to multiple sclerosis (MS) is in part genetically determined. Likewise the heterogeneity in clinical manifestations, temporal course, severity, and in the pathological processes of MS are probably also influenced by our genes. Apolipoprotein E (apoE) polymorphism has been considered a candidate for impacting on MS because of its numerous functions related to brain tissue and evidence for an association with a variety of cerebral disorders, specifically Alzheimer's disease (AD). The apoE alleles epsilon2, epsilon3, and epsilon4 are known to impact differently on aspects such as neuronal growth and repair, neuroprotection and inflammation. After a review of the strong association of the apoE polymorphism with AD, we review the results on MS. These are far less homogenous but have gained support from morphologic and metabolic measures obtained with magnetic resonance imaging indicating a greater extent of brain destruction with the apoE epsilon4 allele. Evidence for a protective role of the epsilon2 allele in MS is weak. In view of the association with AD it is tempting to speculate that neuropsychologic functioning in MS might be even more strongly related to the apoE polymorphism and especially to the epsilon4 allele than other deficits, but few data on this issue are yet available. While part of the association of the apoE polymorphism with AD is supposed to be caused by apoE-isoform dependent effects on amyloid-beta deposition, no single pathogenetically relevant mechanism has yet been confirmed for MS. In summary we presently may assume only subtle effects of the apoE polymorphism on the course of MS. These effects are probably further modulated by other genes and need further investigation.
Find related publications in this database (using NLM MeSH Indexing)
Alzheimer Disease - epidemiology
Animals - epidemiology
Apolipoproteins E - genetics
Humans - genetics
Multiple Sclerosis - epidemiology
Polymorphism, Genetic - epidemiology
Risk - epidemiology

Find related publications in this database (Keywords)
multiple sclerosis
apolipoprotein e polymorphism
Alzheimer disease
magnetic resonance imaging
© Med Uni Graz Impressum