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Neuropathological characterization of mutant amyloid precursor protein yeast artificial chromosome transgenic mice.
Neurobiol Dis 2001; 8(6):982-92ND

Abstract

Mutations in the amyloid precursor protein (APP) gene result in elevated production and deposition of the 42 amino acid beta-amyloid (Abeta1-42) peptide and early-onset Alzheimer's disease (AD). To accurately examine the effect of the APP FAD mutations in vivo, we introduced yeast artificial chromosomes (YACs) containing the entire genomic copy of human APP harboring FAD mutations into transgenic mice. Our current results demonstrate that mutant APP YAC transgenic mice exhibit many features characteristic of human AD, including regional deposition of Abeta with preferential deposition of Abeta1-42, extensive neuritic abnormalities as evidenced by staining with APP, ubiquitin, neurofilament, and hyperphosphorylated tau antibodies, increased markers of inflammation, and the overlapping deposition of Abeta with apolipoproteins E and J. Our results also suggest that APP YAC transgenic mice possess unique pathological attributes when compared to other transgenic mouse models of AD that may reflect the experimental design of each model.

Authors+Show Affiliations

Department of Genetics and Neuroscience, Case Western Reserve University and Center for Human Genetics, Cleveland, Ohio 44106, USA.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

11741394

Citation

Kulnane, L S., and B T. Lamb. "Neuropathological Characterization of Mutant Amyloid Precursor Protein Yeast Artificial Chromosome Transgenic Mice." Neurobiology of Disease, vol. 8, no. 6, 2001, pp. 982-92.
Kulnane LS, Lamb BT. Neuropathological characterization of mutant amyloid precursor protein yeast artificial chromosome transgenic mice. Neurobiol Dis. 2001;8(6):982-92.
Kulnane, L. S., & Lamb, B. T. (2001). Neuropathological characterization of mutant amyloid precursor protein yeast artificial chromosome transgenic mice. Neurobiology of Disease, 8(6), pp. 982-92.
Kulnane LS, Lamb BT. Neuropathological Characterization of Mutant Amyloid Precursor Protein Yeast Artificial Chromosome Transgenic Mice. Neurobiol Dis. 2001;8(6):982-92. PubMed PMID: 11741394.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuropathological characterization of mutant amyloid precursor protein yeast artificial chromosome transgenic mice. AU - Kulnane,L S, AU - Lamb,B T, PY - 2001/12/14/pubmed PY - 2002/2/22/medline PY - 2001/12/14/entrez SP - 982 EP - 92 JF - Neurobiology of disease JO - Neurobiol. Dis. VL - 8 IS - 6 N2 - Mutations in the amyloid precursor protein (APP) gene result in elevated production and deposition of the 42 amino acid beta-amyloid (Abeta1-42) peptide and early-onset Alzheimer's disease (AD). To accurately examine the effect of the APP FAD mutations in vivo, we introduced yeast artificial chromosomes (YACs) containing the entire genomic copy of human APP harboring FAD mutations into transgenic mice. Our current results demonstrate that mutant APP YAC transgenic mice exhibit many features characteristic of human AD, including regional deposition of Abeta with preferential deposition of Abeta1-42, extensive neuritic abnormalities as evidenced by staining with APP, ubiquitin, neurofilament, and hyperphosphorylated tau antibodies, increased markers of inflammation, and the overlapping deposition of Abeta with apolipoproteins E and J. Our results also suggest that APP YAC transgenic mice possess unique pathological attributes when compared to other transgenic mouse models of AD that may reflect the experimental design of each model. SN - 0969-9961 UR - https://www.unboundmedicine.com/medline/citation/11741394/Neuropathological_characterization_of_mutant_amyloid_precursor_protein_yeast_artificial_chromosome_transgenic_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0969-9961(01)90446-2 DB - PRIME DP - Unbound Medicine ER -