Tags

Type your tag names separated by a space and hit enter

The angiotensin 1-converting enzyme insertion (I)/deletion (D) polymorphism does not influence the extent of amyloid or tau pathology in patients with sporadic Alzheimer's disease.

Abstract

An insertion (I)/deletion (D) polymorphism in the angiotensin 1-converting enzyme (ACE) gene has, in some studies, been associated with increased risk for Alzheimer's disease (AD), and functionally the enzyme has been implicated in the degradation of amyloid beta protein (Abeta). We have investigated the frequency of the I/D polymorphism in a clinic-based and autopsy-confirmed series of cases of AD, and investigated what impact the I/D polymorphism in ACE gene might have on the extent of Abeta and tau pathology in the frontal cortex in the autopsy-confirmed series. We found no differences in I/D allele or genotype frequencies between the clinic-based and autopsy-confirmed AD cases, or between the pooled clinic-based and autopsy-confirmed AD cases and a series of normal control subjects. Moreover, Abeta (Abeta(40) and Abeta(42)) load, tau load or extent of amyloid angiopathy did not differ between D/D, I/D and I/I genotype groups, though Abeta(42) load tended to be higher in bearers of I/I genotype (compared to D/D genotype). Neither age at onset nor duration of illness differed according to genotype. We conclude therefore that the frequency of ACE I-allele is not increased in AD and, in autopsy-confirmed AD cases, possession of the ACE I allele has no impact upon the pathology of AD, at least in terms of the amount of Abeta or tau deposited in the brain.

Links

  • Publisher Full Text
  • Authors+Show Affiliations

    ,

    Department of Psychiatry, University of Birmingham, Birmingham B15 2QZ, UK.

    , , , , , , ,

    Source

    Neuroscience letters 328:3 2002 Aug 16 pg 314-8

    MeSH

    Aged
    Aged, 80 and over
    Alleles
    Alzheimer Disease
    Amyloid beta-Peptides
    Apolipoprotein E4
    Apolipoproteins E
    Brain
    DNA Transposable Elements
    Female
    Gene Deletion
    Gene Frequency
    Genotype
    Humans
    Male
    Middle Aged
    Peptide Fragments
    Peptidyl-Dipeptidase A
    Polymorphism, Genetic
    Reference Values
    tau Proteins

    Pub Type(s)

    Journal Article

    Language

    eng

    PubMed ID

    12147333

    Citation

    Lendon, C L., et al. "The Angiotensin 1-converting Enzyme Insertion (I)/deletion (D) Polymorphism Does Not Influence the Extent of Amyloid or Tau Pathology in Patients With Sporadic Alzheimer's Disease." Neuroscience Letters, vol. 328, no. 3, 2002, pp. 314-8.
    Lendon CL, Thaker U, Harris JM, et al. The angiotensin 1-converting enzyme insertion (I)/deletion (D) polymorphism does not influence the extent of amyloid or tau pathology in patients with sporadic Alzheimer's disease. Neurosci Lett. 2002;328(3):314-8.
    Lendon, C. L., Thaker, U., Harris, J. M., McDonagh, A. M., Lambert, J. C., Chartier-Harlin, M. C., ... Mann, D. M. (2002). The angiotensin 1-converting enzyme insertion (I)/deletion (D) polymorphism does not influence the extent of amyloid or tau pathology in patients with sporadic Alzheimer's disease. Neuroscience Letters, 328(3), pp. 314-8.
    Lendon CL, et al. The Angiotensin 1-converting Enzyme Insertion (I)/deletion (D) Polymorphism Does Not Influence the Extent of Amyloid or Tau Pathology in Patients With Sporadic Alzheimer's Disease. Neurosci Lett. 2002 Aug 16;328(3):314-8. PubMed PMID: 12147333.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - The angiotensin 1-converting enzyme insertion (I)/deletion (D) polymorphism does not influence the extent of amyloid or tau pathology in patients with sporadic Alzheimer's disease. AU - Lendon,C L, AU - Thaker,U, AU - Harris,J M, AU - McDonagh,A M, AU - Lambert,J-C, AU - Chartier-Harlin,M-C, AU - Iwatsubo,T, AU - Pickering-Brown,S M, AU - Mann,D M A, PY - 2002/7/31/pubmed PY - 2002/10/29/medline PY - 2002/7/31/entrez SP - 314 EP - 8 JF - Neuroscience letters JO - Neurosci. Lett. VL - 328 IS - 3 N2 - An insertion (I)/deletion (D) polymorphism in the angiotensin 1-converting enzyme (ACE) gene has, in some studies, been associated with increased risk for Alzheimer's disease (AD), and functionally the enzyme has been implicated in the degradation of amyloid beta protein (Abeta). We have investigated the frequency of the I/D polymorphism in a clinic-based and autopsy-confirmed series of cases of AD, and investigated what impact the I/D polymorphism in ACE gene might have on the extent of Abeta and tau pathology in the frontal cortex in the autopsy-confirmed series. We found no differences in I/D allele or genotype frequencies between the clinic-based and autopsy-confirmed AD cases, or between the pooled clinic-based and autopsy-confirmed AD cases and a series of normal control subjects. Moreover, Abeta (Abeta(40) and Abeta(42)) load, tau load or extent of amyloid angiopathy did not differ between D/D, I/D and I/I genotype groups, though Abeta(42) load tended to be higher in bearers of I/I genotype (compared to D/D genotype). Neither age at onset nor duration of illness differed according to genotype. We conclude therefore that the frequency of ACE I-allele is not increased in AD and, in autopsy-confirmed AD cases, possession of the ACE I allele has no impact upon the pathology of AD, at least in terms of the amount of Abeta or tau deposited in the brain. SN - 0304-3940 UR - https://www.unboundmedicine.com/medline/citation/12147333/The_angiotensin_1_converting_enzyme_insertion__I_/deletion__D__polymorphism_does_not_influence_the_extent_of_amyloid_or_tau_pathology_in_patients_with_sporadic_Alzheimer's_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304394002005530 DB - PRIME DP - Unbound Medicine ER -