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Morphological, Biochemical, and Genetic Support for an Apolipoprotein E Effect on Microtubular Metabolism a
Author(s) -
ROSES A. D.,
EINSTEIN G.,
GILBERT J.,
GOEDERT M.,
HAN SH.,
HUANG D.,
HULETTE C.,
MASLIAH E.,
PERICAKVANCE M. A.,
SAUNDERS A. M.,
SCHMECHEL D. E.,
STRITTMATTTER W. J.,
WEISGRABER K. H.,
XI P.T.
Publication year - 1996
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1996.tb34413.x
Subject(s) - apolipoprotein e , biology , chemistry , genetics , medicine , disease
There are two distinct viewpoints on the association of the inheritance of apolipoprotein E (APOE) alleles and the age of onset distribution of Alzheimer's disease (AD): genetic and phenotypic expression. There have been multiple corroborations of the APOE‐ε4 association with Alzheimer's disease in populations around the world in clinic based studies as well as emerging epidemiological studies. The genetic data do not imply mechanism of pathogenesis. The phenotypic expression of AD has been based in theories based on amyloid plaques or neurofibrillary tangles. ApoE protein interacts with both β‐amyloid and tau in an isoform‐specific manner. The interaction with tau had been thought to be an in vitro artifact, since apoE had not been previously localized to the