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Angiotensin converting enzyme insertion/deletion polymorphism in sporadic and familial Alzheimer's disease and longevity.

Abstract

A recent, large meta-analysis has reproposed the role of the angiotensin converting enzyme (ACE) insertion/deletion (I/D) polymorphism as a risk factor for Alzheimer's disease (AD). To further investigate the proposed association and to better clarify the role of ACE as a risk factor for AD, we analyzed the genotype and allele frequency distribution of ACE I/D and apolipoprotein E (APOE) gene polymorphisms in 235 Italian patients with sporadic AD, 153 with familial AD (FAD), 192 healthy controls and 111 centenarians. Patients with AD were consecutively gathered from among the outpatients from the Neurology Department at the University of Florence. All 691 subjects were genotyped for ACE and APOE polymorphisms. There were no significant differences in ACE genotypes or allele frequencies in all the studied groups, even after stratification for APOE epsilon4 carrier status. Centenarians show the highest allele D frequency, although the value is not significant, thus suggesting a possible implication of the D allele as an epistatic allele that has pleiotropic age-dependent effects. In conclusion, our data suggest that the ACE allelic variant is not a susceptibility factor in sporadic and familial AD (FAD), nor does it mitigate the effect of the APOE epsilon4 allele in the risk of developing AD. Moreover, our data do not suggest a possible involvement of the D allele in longevity.

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  • Authors+Show Affiliations

    ,

    Department of Neurological and Psychiatric Sciences, University of Florence, Florence and Centro di Ricerca, Trasferimento e Alta Formazione DENOTHE, University of Florence, Viale Morgagni, 85, 50134 Firenze, Italy. nacmias@unifi.it

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    Source

    MeSH

    Aged
    Aged, 80 and over
    Alzheimer Disease
    Apolipoprotein E4
    Case-Control Studies
    Female
    Gene Frequency
    Genetic Predisposition to Disease
    Genotype
    Humans
    Italy
    Longevity
    Male
    Middle Aged
    Mutation
    Peptidyl-Dipeptidase A
    Polymerase Chain Reaction
    Polymorphism, Genetic
    Sequence Deletion

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    17182125

    Citation

    Nacmias, Benedetta, et al. "Angiotensin Converting Enzyme Insertion/deletion Polymorphism in Sporadic and Familial Alzheimer's Disease and Longevity." Archives of Gerontology and Geriatrics, vol. 45, no. 2, 2007, pp. 201-6.
    Nacmias B, Bagnoli S, Tedde A, et al. Angiotensin converting enzyme insertion/deletion polymorphism in sporadic and familial Alzheimer's disease and longevity. Arch Gerontol Geriatr. 2007;45(2):201-6.
    Nacmias, B., Bagnoli, S., Tedde, A., Cellini, E., Bessi, V., Guarnieri, B., ... Sorbi, S. (2007). Angiotensin converting enzyme insertion/deletion polymorphism in sporadic and familial Alzheimer's disease and longevity. Archives of Gerontology and Geriatrics, 45(2), pp. 201-6.
    Nacmias B, et al. Angiotensin Converting Enzyme Insertion/deletion Polymorphism in Sporadic and Familial Alzheimer's Disease and Longevity. Arch Gerontol Geriatr. 2007;45(2):201-6. PubMed PMID: 17182125.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Angiotensin converting enzyme insertion/deletion polymorphism in sporadic and familial Alzheimer's disease and longevity. AU - Nacmias,Benedetta, AU - Bagnoli,Silvia, AU - Tedde,Andrea, AU - Cellini,Elena, AU - Bessi,Valentina, AU - Guarnieri,Biancamaria, AU - Ortensi,Luigi, AU - Piacentini,Silvia, AU - Bracco,Laura, AU - Sorbi,Sandro, Y1 - 2006/12/19/ PY - 2006/05/26/received PY - 2006/10/16/revised PY - 2006/10/20/accepted PY - 2006/12/22/pubmed PY - 2007/10/19/medline PY - 2006/12/22/entrez SP - 201 EP - 6 JF - Archives of gerontology and geriatrics JO - Arch Gerontol Geriatr VL - 45 IS - 2 N2 - A recent, large meta-analysis has reproposed the role of the angiotensin converting enzyme (ACE) insertion/deletion (I/D) polymorphism as a risk factor for Alzheimer's disease (AD). To further investigate the proposed association and to better clarify the role of ACE as a risk factor for AD, we analyzed the genotype and allele frequency distribution of ACE I/D and apolipoprotein E (APOE) gene polymorphisms in 235 Italian patients with sporadic AD, 153 with familial AD (FAD), 192 healthy controls and 111 centenarians. Patients with AD were consecutively gathered from among the outpatients from the Neurology Department at the University of Florence. All 691 subjects were genotyped for ACE and APOE polymorphisms. There were no significant differences in ACE genotypes or allele frequencies in all the studied groups, even after stratification for APOE epsilon4 carrier status. Centenarians show the highest allele D frequency, although the value is not significant, thus suggesting a possible implication of the D allele as an epistatic allele that has pleiotropic age-dependent effects. In conclusion, our data suggest that the ACE allelic variant is not a susceptibility factor in sporadic and familial AD (FAD), nor does it mitigate the effect of the APOE epsilon4 allele in the risk of developing AD. Moreover, our data do not suggest a possible involvement of the D allele in longevity. SN - 0167-4943 UR - https://www.unboundmedicine.com/medline/citation/17182125/Angiotensin_converting_enzyme_insertion/deletion_polymorphism_in_sporadic_and_familial_Alzheimer's_disease_and_longevity_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0167-4943(06)00123-3 DB - PRIME DP - Unbound Medicine ER -