FAMILIAL AND SPORADIC ALZHEIMERS-DISEASE - NEUROPATHOLOGY CANNOT EXCLUDE A FINAL COMMON PATHWAY

Citation
Cf. Lippa et al., FAMILIAL AND SPORADIC ALZHEIMERS-DISEASE - NEUROPATHOLOGY CANNOT EXCLUDE A FINAL COMMON PATHWAY, Neurology, 46(2), 1996, pp. 406-412
Citations number
70
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00283878
Volume
46
Issue
2
Year of publication
1996
Pages
406 - 412
Database
ISI
SICI code
0028-3878(1996)46:2<406:FASA-N>2.0.ZU;2-X
Abstract
Whether all etiologic forms of Alzheimer's disease (AD) share a final common pathway is a major issue, We determined the severity and region al distribution of neuronal loss, amyloid plaques, neuritic plaques (N Ps), and neurofibrillary tangles (NFTs), and calculated the ratio of n euronal loss to NPs and NFTs in brains of 19 familial AD (FAD) patient s with linkage to chromosome 14, six AD patients with mutations of chr omosome 21 (codon 717 of the beta-amyloid precursor 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 cou ld be distinguished from SAD by the greater severity and the lack of i nfluence of apolipoprotein E genotype on pathology, These differences may reflect differences in age at onset rather than different etiopath ologic mechanisms, The similarity of pathologic findings in the differ ent AD groups provides evidence for a final common pathophysiologic pa thway in AD.