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@ARTICLE{Meyer:285731,
author = {Meyer, Charlotte Clara and de Mattos, Eduardo Preusser and
Burger, Rahel Maria and Blumenstock, Gunnar and Pereira
Sena, Priscila and Gordon, Carlos and Zaltzman, Roy and
França, Marcondes Cavalcante and Saraiva-Pereira,
Maria-Luiza and Cornejo-Olivas, Mario R and Bauer, Peter and
Schöls, Ludger and van de Warrenburg, Bart P and Durr,
Alexandra and Brice, Alexis and Klockgether, Thomas and
Jardim, Laura Bannach and Riess, Olaf and Schmidt, Thorsten},
collaboration = {Network, EUROSCA},
othercontributors = {Bauer, Peter and Berciano, José and Boesch, Sylvia and
Brice, Alexis and Durr, Alexandra and Forlani, Sylvie and
Giunti, Paola and Jacobi, Heike and Klockgether, Thomas and
Melegh, Bela and Pandolfo, Massimo and Riess, Olaf and
Schmitz-Hübsch, Tanja and Schöls, Ludger and Schulz, Jörg
B and Stevanin, Giovanni and Szymanski, Sandra and du
Montcel, Sophie Tezenas and Timmann, Dagmar and van de
Warrenburg, Bart P C},
title = {{A}ssociation of rare apolipoprotein {E} ε4 homozygosity
with an earlier age at onset in spinocerebellar ataxia type
3.},
journal = {Human molecular genetics},
volume = {35},
number = {5},
issn = {0964-6906},
address = {Oxford},
publisher = {Oxford Univ. Press},
reportid = {DZNE-2026-00288},
pages = {ddag016},
year = {2026},
abstract = {Spinocerebellar Ataxia Type 3 (SCA3) is an autosomal
dominant neurodegenerative Polyglutamine (polyQ) disease,
caused by a cytosine-adenine-guanine (CAG) repeat expansion
in the ATXN3 gene, resulting in an expanded polyQ tract in
the Ataxin-3 protein. Although the principal genetic
determinant of the age at onset (AAO) in polyQ diseases is
the expanded CAG repeat length, variability in AAO has been
explained only partly, suggesting the existence of
additional genetic modifiers. Apolipoprotein E (APOE)
haplotypes are associated with the risk of numerous,
especially degenerative, diseases. Investigations of a
potential role of APOE haplotypes in AAO variability of SCA3
have resulted in partly conflicting outcomes, with current
evidence lacking power and patient diversity. To further
clarify a potential modifying effect of APOE haplotypes on
the AAO in SCA3, over 800 SCA3 patients from different
origins were enrolled in the present study. While we did not
find an association of common APOE haplotypes or singular
APOE alleles with AAO in SCA3, rare ε4 homozygosity was
linked to an earlier AAO in individuals from Brazil, with a
mean disease onset six years earlier than carriers of other
APOE haplotypes. Our study thus provides initial evidence
for a relevant impact of ε4 homozygosity on disease onset
in SCA3 and provides evidence supporting an allele-dosage
effect of APOE ε4 in polyQ diseases.},
keywords = {Humans / Age of Onset / Female / Male / Machado-Joseph
Disease: genetics / Machado-Joseph Disease: epidemiology /
Middle Aged / Homozygote / Adult / Haplotypes /
Apolipoprotein E4: genetics / Aged / Ataxin-3 / Alleles /
Repressor Proteins / Spinocerebellar Ataxia 3 (Other) /
genetic modifier (Other) / genetic risk factor (Other) /
neurodegeneration (Other) / neurogenetics (Other) /
Apolipoprotein E4 (NLM Chemicals) / Ataxin-3 (NLM Chemicals)
/ ATXN3 protein, human (NLM Chemicals) / Repressor Proteins
(NLM Chemicals)},
cin = {AG Schöls / Patient Studies (Bonn)},
ddc = {570},
cid = {I:(DE-2719)5000005 / I:(DE-2719)1011101},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:41854058},
doi = {10.1093/hmg/ddag016},
url = {https://pub.dzne.de/record/285731},
}