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Transgenic Mice Expressing Human β‐APP751, But Not Mice Expressing β‐APP695, Display Early Alzheimer's Disease‐like Histopathology a
Author(s) -
HIGGINS L. S.,
CATALANO R.,
QUON D.,
CORDELL B.
Publication year - 1993
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.1749-6632.1993.tb23056.x
Subject(s) - enolase , genetically modified mouse , gene isoform , transgene , microbiology and biotechnology , biology , amyloid precursor protein , alzheimer's disease , amyloid (mycology) , stain , antibody , pathology , immunohistochemistry , staining , biochemistry , disease , medicine , gene , immunology
Mice transgenic for the 751 amino acid isoform of the human β‐amyloid precursor protein (β‐APP) driven by the rat neuron specific enolase (NSE) promoter (NSE:β‐APP751) show features of early Alzheimer's disease (AD) pathology. These features, which were evident in multiple pedigrees, include: 1) preamyloid deposits which stain with antibodies that are specific for the β‐amyloid peptide and stain AD amyloid deposits and plaques, and 2) neuronal soma and processes which stain with an antibody (Alz50) that detects abnormal isoforms of tau which are characteristic of AD. The quality and distribution of both types of immunoreactivity revealed in the NSE:β‐APP751 mouse brains most closely resemble those seen in brains of young adults with Down's syndrome. Both structures are rarely, if ever, observed in brains from mice transgenic for the 695 amino acid isoform of β‐APP (NSE:β‐APP695) or in wild type mice.