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Aberrant accentuation of neurofibrillary degeneration in the hippocampus of Alzheimer's disease with amyloid precursor protein 717 and presenilin-1 gene mutations.
J Neurol Sci. 2005 Jul 15; 234(1-2):55-65.JN

Abstract

This study reports correlation of the hippocampal neurofibrillary tangles (NFT) density with beta-amyloid (Abeta) precursor protein (APP) 717 mutation, presenilin (PS)-1 mutation and apolipoprotein E (Apo-E) e4 alleles (E4), being graded as 3 forms (no-E4, one-E4 and two-E4) in autopsied brains from patients with familial and non-familial Alzheimer's disease (AD). We studied the density of NFT-free neurons, intracellular NFT (I-NFT), extracellular NFT (E-NFT) and total NFT (I-NFT plus E-NFT) in the six hippocampal subdivisions: cornu ammonis (CA) 1-CA4, subiculum and entorhinal cortex. The APP mutation cases showed significantly higher total NFT density in the CA1-CA2 region, and the PS-1 mutation cases also showed higher density of total NFT in the CA1-CA3 than non-familial cases. Moreover, high densities of the E-NFT contributed to these high total NFT densities. Non-familial AD cases showed a stereotypical NFT distribution with entorhinal accentuation in the hippocampus irrespective of E4 frequency. Thus, APP and PS-1 mutations predominantly affect the CA regions with profound neurodegeneration, which contributes early and severe clinical features of familial AD.

Authors+Show Affiliations

Department of Neuropsychiatry, Faculty of Medical Sciences, University of Fukui, 23 Shimoaizuki, Matsuoka-cho, Fukui 910-1193, Japan. satorv@fmsrsa.fukui-med.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

15946688

Citation

Sudo, Satoru, et al. "Aberrant Accentuation of Neurofibrillary Degeneration in the Hippocampus of Alzheimer's Disease With Amyloid Precursor Protein 717 and Presenilin-1 Gene Mutations." Journal of the Neurological Sciences, vol. 234, no. 1-2, 2005, pp. 55-65.
Sudo S, Shiozawa M, Cairns NJ, et al. Aberrant accentuation of neurofibrillary degeneration in the hippocampus of Alzheimer's disease with amyloid precursor protein 717 and presenilin-1 gene mutations. J Neurol Sci. 2005;234(1-2):55-65.
Sudo, S., Shiozawa, M., Cairns, N. J., & Wada, Y. (2005). Aberrant accentuation of neurofibrillary degeneration in the hippocampus of Alzheimer's disease with amyloid precursor protein 717 and presenilin-1 gene mutations. Journal of the Neurological Sciences, 234(1-2), 55-65.
Sudo S, et al. Aberrant Accentuation of Neurofibrillary Degeneration in the Hippocampus of Alzheimer's Disease With Amyloid Precursor Protein 717 and Presenilin-1 Gene Mutations. J Neurol Sci. 2005 Jul 15;234(1-2):55-65. PubMed PMID: 15946688.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Aberrant accentuation of neurofibrillary degeneration in the hippocampus of Alzheimer's disease with amyloid precursor protein 717 and presenilin-1 gene mutations. AU - Sudo,Satoru, AU - Shiozawa,Masaki, AU - Cairns,Nigel J, AU - Wada,Yuji, PY - 2004/12/17/received PY - 2005/02/24/revised PY - 2005/03/08/accepted PY - 2005/6/11/pubmed PY - 2005/9/20/medline PY - 2005/6/11/entrez SP - 55 EP - 65 JF - Journal of the neurological sciences JO - J. Neurol. Sci. VL - 234 IS - 1-2 N2 - This study reports correlation of the hippocampal neurofibrillary tangles (NFT) density with beta-amyloid (Abeta) precursor protein (APP) 717 mutation, presenilin (PS)-1 mutation and apolipoprotein E (Apo-E) e4 alleles (E4), being graded as 3 forms (no-E4, one-E4 and two-E4) in autopsied brains from patients with familial and non-familial Alzheimer's disease (AD). We studied the density of NFT-free neurons, intracellular NFT (I-NFT), extracellular NFT (E-NFT) and total NFT (I-NFT plus E-NFT) in the six hippocampal subdivisions: cornu ammonis (CA) 1-CA4, subiculum and entorhinal cortex. The APP mutation cases showed significantly higher total NFT density in the CA1-CA2 region, and the PS-1 mutation cases also showed higher density of total NFT in the CA1-CA3 than non-familial cases. Moreover, high densities of the E-NFT contributed to these high total NFT densities. Non-familial AD cases showed a stereotypical NFT distribution with entorhinal accentuation in the hippocampus irrespective of E4 frequency. Thus, APP and PS-1 mutations predominantly affect the CA regions with profound neurodegeneration, which contributes early and severe clinical features of familial AD. SN - 0022-510X UR - https://www.unboundmedicine.com/medline/citation/15946688/Aberrant_accentuation_of_neurofibrillary_degeneration_in_the_hippocampus_of_Alzheimer's_disease_with_amyloid_precursor_protein_717_and_presenilin_1_gene_mutations_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-510X(05)00112-7 DB - PRIME DP - Unbound Medicine ER -