Title

Familial and sporadic Alzheimer's disease: neuropathology cannot exclude a final common pathway

UMMS Affiliation

Department of Neurology

Date

2-1-1996

Document Type

Article

Subjects

Age of Onset; Aged; Alleles; Alzheimer Disease; Amyloid; Amyloid beta-Protein Precursor; Analysis of Variance; Apolipoproteins E; Brain; Cerebellum; Chromosomes, Human, Pair 14; Chromosomes, Human, Pair 21; Gene Frequency; Humans; Linkage (Genetics); Middle Aged; Mutation; Neurites; Neurofibrillary Tangles; Neurons; Organ Specificity

Disciplines

Neurology | Neuroscience and Neurobiology

Abstract

Whether all etiologic forms of Alzheimer's disease (AD) share a final common pathway is a major issue. We determined the severity and regional distribution of neuronal loss, amyloid plaques, neuritic plaques (NPs), and neurofibrillary tangles (NFTs), and calculated the ratio of neuronal loss to NPs and NFTs in brains of 19 familial AD (FAD) patients with linkage to chromosome 14, six AD patients with mutations of chromosome 21 (codon 717 of the beta-amyloid percursor protein gene), and 11 sporadic AD (SAD) patients. There was no difference in the pattern of distribution of the various pathologic features or in the ratio of neuronal loss to NPs or NFTs in any AD group. However, FAD groups could be distinguished from SAD by the greater severity and the lack of influence of apolipoprotein E genotype on pathology. These differences may reflect differences in age at onset rather than different etiopathologic mechanisms. The similarity of pathologic findings in the different AD groups provides evidence for a final common pathophysiologic pathway in AD.

Rights and Permissions

Citation: Neurology. 1996 Feb;46(2):406-12.

Related Resources

Link to Article in PubMed

PubMed ID

8614503

This document is currently not available here.

Share

COinS