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Apolipoprotein E allele 4 is not a sufficient or a necessary predictor of the development of Mild Cognitive Impairment

Published online by Cambridge University Press:  16 April 2020

R. Heun ,
U. Gühne ,
T. Luck ,
M.C. Angermeyer ,
U. Ueberham ,
R. Potluri ,
A. Natalwala ,
T. Arendt  and
S.G. Riedel-Heller
R. Heun*
Affiliation:
Department of Psychiatry, Derby City General Hospital, Uttoxeter Road, Derby22, UK
U. Gühne
Affiliation:
Department of Psychiatry, Public Mental Health Research Unit, University of Leipzig, Liepzig, Germany
T. Luck
Affiliation:
Department of Psychiatry, Public Mental Health Research Unit, University of Leipzig, Liepzig, Germany
M.C. Angermeyer
Affiliation:
Department of Psychiatry, Public Mental Health Research Unit, University of Leipzig, Liepzig, Germany
U. Ueberham
Affiliation:
Paul-Flechsig Institute of Brain Research, Leipzig, Germany
R. Potluri
Affiliation:
Faculty of Medicine, Imperial College, London, UK
A. Natalwala
Affiliation:
The Medical School, University of Birmingham, Birmingham, UK
T. Arendt
Affiliation:
Paul-Flechsig Institute of Brain Research, Leipzig, Germany
S.G. Riedel-Heller
Affiliation:
Department of Psychiatry, Public Mental Health Research Unit, University of Leipzig, Liepzig, Germany
*
*Auteur correspondant. Tel.: +44 7595 635638. E-mail address: [email protected] (R. Heun).
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Abstract

The presence of Mild Cognitive Impairment (MCI) and of an apolipoprotein E (apoE) ε4 allele both predict the development of Alzheimer's disease. However, the extent to which this allele also predicts the development of MCI is unclear even though MCI is an early transitional stage in the development of Alzheimer's disease. The present study investigates the prevalence of the apoE ε4 allele in incipient MCI. Participants were recruited from the population-based Leipzig Longitudinal Study of the Aged (LEILA75+). All subjects who were initially cognitively healthy, i.e. did not meet MCI criteria described by Petersen [Petersen RC. Mild cognitive impairment. J Intern Med 2004; 256(3): 183–94], and whose apoE status could be determined were followed-up. After 4.5 years, 15.5% of the cognitively healthy target population had developed MCI. The frequencies of the apoE ε4 genotype did not differ between individuals with incipient MCI (12.9%) and individuals who remained cognitively healthy during the study (18.4%, p > 0.5). Consequently, the apoE ε4 genotype is not a necessary or sufficient risk factor for MCI. Further studies need to investigate the influence of the whole range of genetic and environmental risk factors on the course of Alzheimer's disease including the initial development of MCI and the later conversion to Alzheimer's disease.

Keywords

Mild cognitive impairmentIncidenceApolipoprotein EEpidemiologyConversionAlzheimer's disease
Type
Original articles
Information
European Psychiatry , Volume 25 , Issue 1 , January 2010 , pp. 15 - 18
Copyright
Copyright © Elsevier Masson SAS 2010

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References

Bartrés-Faz, D., Clemente, I.C., Junqué, C., Valveny, N., López-Alomar, A., Sánchez-Aldeguer, J.et al. APOE and APOC1 genetic polymorphisms in age-associated memory impairment. Neurogenetics 2001 3(4)215–219.Google ScholarPubMed
Chapman, J., Estupiñan, J., Asherov, A., Goldfarb, L.G.A simple and efficient method for apolipoprotein E genotype determination. Neurology 1996 46(5)1484–1485.CrossRefGoogle ScholarPubMed
Chiappelli, M., Borroni, B., Archetti, S., Calabrese, E., Corsi, M.M., Franceschi, M.et al. VEGF gene and phenotype relation with Alzheimer's disease and mild cognitive impairment. Rejuvenation Res 2006 9(4)485–493.CrossRefGoogle ScholarPubMed
Collie, A., Maruff, P., Currie, J.Behavioral characterization of mild cognitive impairment. J Clin Exp Neuropsychol 2002 24(6)720–733.CrossRefGoogle ScholarPubMed
Devanand, D.P., Pelton, G.H., Zamora, D., Liu, X., Tabert, M.H., Goodkind, M.et al. Predictive utility of apolipoprotein E genotype for Alzheimer disease in outpatients with mild cognitive impairment. Arch Neurol 2005 62(6)975–980.CrossRefGoogle ScholarPubMed
Farrer, L.A., Cupples, L.A., Haines, J.L., Hyman, B., Kukull, W.A., Mayeux, R.et al. Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. A meta-analysis. APOE and Alzheimer Disease Meta Analysis Consortium. J Am Med Assoc 1997 278(16)1349–1356.CrossRefGoogle ScholarPubMed
Förstl, H., Hentschel, F., Sattel, H., Geiger-Kabisch, C., Besthorn, C., Czech, C.et al. Age-associated memory impairment and early Alzheimer's disease. Only time will tell the difference. Arzneimittelforschung 1995 45(3A)394–397.Google ScholarPubMed
Heun, R., Papassotiropoulos, A., Jessen, F., Maier, W., Breitner, J.C.A family study of Alzheimer disease and early–and late-onset depression in elderly patients. Arch Gen Psychiatry 2001 58(2)190–196.CrossRefGoogle ScholarPubMed
Heun, R., Ptok, U., Kölsch, H., Maier, W., Jessen, F.Contribution of apolipoprotein E and cathepsin D genotypes to the familial aggregation of Alzheimer's disease. Dement Geriatr Cogn Disord 2004 18(2)151–158.CrossRefGoogle ScholarPubMed
Hsiung, G.Y., Sadovnick, A.D., Feldman, H.Apolipoprotein E epsilon4 genotype as a risk factor for cognitive decline and dementia: data from the Canadian Study of Health and Aging. CMAJ 2004 171(8)863–867.CrossRefGoogle ScholarPubMed
Lautenschlager, N., Kurz, A., Müller, U.Inheritable causes and risk factors of Alzheimer's disease. Nervenarzt 1999 70(3)195–205.CrossRefGoogle ScholarPubMed
Lopez, O.L., Jagust, W.J., DeKosky, S.T., Becker, J.T., Fitzpatrick, A., Dulberg, C.et al. Prevalence and classification of mild cognitive impairment in the Cardiovascular Health Study Cognition Study: part 1. Arch Neurol 2003 60(10)1385–1389.CrossRefGoogle ScholarPubMed
Lopez, O.L., Jagust, W.J., Dulberg, C., Becker, J.T., DeKosky, S.T., Fitzpatrick, A.et al. Risk factors for mild cognitive impairment in the Cardiovascular Health Study Cognition Study: part 2. Arch Neurol 2003 60(10)1394–1399.CrossRefGoogle ScholarPubMed
Maioli, F., Coveri, M., Pagni, P., Chiandetti, C., Marchetti, C., Ciarrocchi, R.et al. Conversion of mild cognitive impairment to dementia in elderly subjects: a preliminary study in a memory and cognitive disorder unit. Arch Gerontol Geriatr 44(Suppl. 1)2007 233–241.CrossRefGoogle Scholar
Petersen, R.C.Mild cognitive impairment as a diagnostic entity. J Intern Med 256(3)2004 183–194.CrossRefGoogle ScholarPubMed
Radloff, L.S.The CES-D Scale: A Self-report Depression Scale for research in the general population. Appl Psychol Meas 1977 1(3)385–401.CrossRefGoogle Scholar
Riedel-Heller, S.G., Busse, A., Aurich, C., Matschinger, H., Angermeyer, M.C.Prevalence of dementia according to DSM-III-R and ICD-10: results of the Leipzig Longitudinal Study of the Aged (LEILA75+) Part 1. Br J Psychiatry 2001;179:250–254.CrossRefGoogle ScholarPubMed
Sando, S.B., Melquist, S., Cannon, A., Hutton, M.L., Sletvold, O., Saltvedt, I.et al. APOE epsilon 4 lowers age at onset and is a high risk factor for Alzheimer's disease; a case control study from central Norway. BMC Neurol 2008;8:9.CrossRefGoogle ScholarPubMed
Spitzer, R.L., Williams, J.B.W., Gibbon, M.Structured clinical interview for DSM-III-R (SCID). Biometric research department New York: NYS Psychiatric Institute; 1987.Google Scholar
Tervo, S., Kivipelto, M., Hänninen, T., Vanhanen, M., Hallikainen, M., Mannermaa, A.et al. Incidence and risk factors for mild cognitive impairment: a population-based three-year follow-up study of cognitively healthy elderly subjects. Dement Geriatr Cogn Disord 2004 17(3)196–203.CrossRefGoogle ScholarPubMed
Traykov, L., Rigaud, A.S., Baudic, S., Smagghe, A., Boller, F., Forette, F.Apolipoprotein E epsilon 4 allele frequency in demented and cognitively impaired patients with and without cerebrovascular disease. J Neurol Sci 2002 203–204177–181.CrossRefGoogle ScholarPubMed
Tsuang, D., Kukull, W., Sheppard, L., Barnhart, R.L., Peskind, E., Edland, S.D.et al. Impact of sample selection on APOE epsilon 4 allele frequency: a comparison of two Alzheimer's disease samples. J Am Geriatr Soc 1996 44(6)704–707.CrossRefGoogle ScholarPubMed
van Duijn, C.M.Prospects of genetic research of mild cognitive impairment. J Intern Med 2004;256:235–239.CrossRefGoogle ScholarPubMed
Waring, S.C., Rosenberg, R.N.Genome-wide association studies in Alzheimer disease. Arch Neurol 2008 65(3)329–334.CrossRefGoogle ScholarPubMed
Zaudig, M., Mittelhammer, J., Hiller, W., Pauls, A., Thora, C., Morinigo, A.et al. SIDAM–A structured interview for the diagnosis of dementia of the Alzheimer type, multi-infarct dementia and dementias of other aetiology according to ICD-10 and DSM-III-R. Psychol Med 1991 21(1)225–236.CrossRefGoogle Scholar
Zill, P., Engel, R., Hampel, H., Behrens, S., Bürger, K., Padberg, F.et al. Polymorphisms in the apolipoprotein E (APOE) gene in gerontopsychiatric patients. Eur Arch Psychiatry Clin Neurosci 2001 251(1)24–28.CrossRefGoogle ScholarPubMed
Zivelin, A., Rosenberg, N., Peretz, H., Amit, Y., Kornbrot, N., Seligsohn, U.Improved method for genotyping apolipoprotein E polymorphisms by a PCR-based assay simultaneously utilizing two distinct restriction enzymes. Clin Chem 1997 43(9)1657–1659.CrossRefGoogle ScholarPubMed
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