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Apolipoprotein E genotypes do not influence the age of onset in Huntington’s disease

¹ Huntington Center NRW, Department of Neurology, St Josef Hospital, Ruhr-University Bochum, Germany
² Huntington Center NRW, Department of Human Genetics, Ruhr-University Bochum, Germany

Correspondence to:
Correspondence to:
Dr J E Andrich
Department of Neurology, St Josef Hospital, Ruhr-University Bochum, Gudrunstr. 56, D-44791 Bochum, Germany; jurgen.andrich{at}ruhr-uni.de

Objective: The 4 allele of the apolipoprotein E (ApoE) gene has been defined as a critical factor for early onset neurodegeneration in Pick’s, Parkinson’s, and Alzheimer’s disease. Unexpectedly, the 4 allele appeared to delay the age of onset in Huntington’s disease (HD) patients. Furthermore, sex specific effects were reported on earlier age of onset due to the ApoE 23 genotype in males with HD. The age of onset of HD is known to be negatively correlated with increasing lengths of pathogenetic CAG expansions in the huntingtin gene.

Methods: In order to examine the effects of CAG block lengths, we have correlated ApoE genotypes with the age of onset in 145 patients symptomatic for HD with psychiatric and somatic symptoms (depression, psychosis, dementia, choreic, and other movement disorders) harbouring only modestly expanded huntingtin alleles (41–45 CAGs).

Results: The negative correlation between age of onset and CAG block length was established in our HD cohort. Statistically significant effects of the 4 allele were not obvious regarding clinical characteristics including age of onset, nor were any sex differences for the 23 genotype observed.

Conclusion: The ApoE genotype does not affect the course of HD significantly.

Abbreviations: AD, Alzheimer’s disease; ApoE, apolipoprotein E; HD, Huntington’s disease; UHDRS, Unified Huntington’s Disease Rating Scale

Keywords: apolipoprotein E; dementia; Huntington’s disease; onset; polymorphism

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