Odor identification impairment in carriers of ApoE-epsilon 4 is independent of clinical dementia
2010 (English)In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 31, no 4, 567-577 p.Article in journal (Refereed) Published
The ApoE acme is expressed in olfactory brain structures and is believed to play a role in neuronal regenerative processes as well as in development of Alzheimer's disease (AD), the most common form of dementia The epsilon 4 allele lots been reported to be associated with compromised odor identification ability in the elderly, and this deficit has been interpreted as a sign of pre-diagnostic AD However, because it has not been demonstrated that the relationship between the epsilon 4 allele and odor identification is mediated by dementia, it is possible that the epsilon 4 allele may have an effect on odor identification over and above any effects of dementia. The present study investigated effects of ApoE-status on odor identification in a lame, population-based sample (n =1236) of adults (45-80 years), who were assessed for dementia at time of testing and 5 years later The results showed that the epsilon 4 allele was associated with an odor identification deficit among, elderly participants (75-80) Critically. this effect remained after current and pre-diagnostic dementia, vocabulary, global cognitive status and health variables were partialled out The present results suggest that the ApoE gene plays a role in olfactory functioning that is independent of dementia conversion within 5 years
Place, publisher, year, edition, pages
2010. Vol. 31, no 4, 567-577 p.
ApoE, Odor identification, Olfaction, Aging, Alzheimer's disease
IdentifiersURN: urn:nbn:se:su:diva-52206DOI: 10.1016/j.neurobiolaging.2008.05.019ISI: 000276759700005OAI: oai:DiVA.org:su-52206DiVA: diva2:387426
The Betula Study is funded by the Bank of Sweden Tercentenary Foundation (1988-0082:17), Swedish Council for Planning and Coordination of Research (D1988-0092, D1989-0115, D1990-0074, D1991-0258, D1992-0143, D1997-0756, D1997-1841, D1999-0739 and B1999-474), Swedish Council for Research in the Humanities and Social Sciences (F377/1988–2000), and the Swedish Council for Social Research (1988–1990: 88-0082 and 311/1991–2000). The authors acknowledge the contribution to this paper of the VIB—Department of Molecular Genetics at the University of Antwerp, Antwerpen, Belgium, and Rolf Adolfsson at the Department of Psychiatry, Umeå University, to the APOE genotyping of Betula individuals. Also, the authors thank Birgitta Törnkvist at the Department of Statistics, Umeå University, for valuable consultation, and six anonymous reviewers for helpful comments. authorCount :62011-01-142011-01-132016-06-22Bibliographically approved