Familial and sporadic Alzheimer's disease: neuropathology cannot exclude a final common pathway
Lippa, Carol F. ; Saunders, Ann M. ; Smith, Thomas W. ; Swearer, Joan M. ; Drachman, David A. ; Ghetti, Bernardino ; Nee, Linda ; Pulaski-Salo, D. ; Dickson, Dennis ; Robitaille, Yves ... show 8 more
Citations
Authors
Saunders, Ann M.
Smith, Thomas W.
Swearer, Joan M.
Drachman, David A.
Ghetti, Bernardino
Nee, Linda
Pulaski-Salo, D.
Dickson, Dennis
Robitaille, Yves
Bergeron, C.
Crain, Barbara
Benson, Merrill D.
Farlow, Martin R.
Hyman, Bradley T.
St. George-Hyslop, Peter H.
Roses, Allen D.
Pollen, Daniel A.
Student Authors
Faculty Advisor
Academic Program
UMass Chan Affiliations
Document Type
Publication Date
Keywords
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
Neurology
Neuroscience and Neurobiology
Subject Area
Embargo Expiration Date
Link to Full Text
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.
Source
Lippa CF, Saunders AM, Smith TW, Swearer JM, Drachman DA, Ghetti B, Nee L, Pulaski-Salo D, Dickson D, Robitaille Y, Bergeron C, Crain B, Benson MD, Farlow M, Hyman BT, George-Hyslop SP, Roses AD, Pollen DA. Familial and sporadic Alzheimer's disease: neuropathology cannot exclude a final common pathway. Neurology. 1996 Feb;46(2):406-12. doi: 10.1212/wnl.46.2.406. PMID: 8614503.