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Systematic Phenotyping and Characterization of the 3xTg-AD Mouse Model of Alzheimer's Disease.
Javonillo, Dominic I; Tran, Kristine M; Phan, Jimmy; Hingco, Edna; Kramár, Enikö A; da Cunha, Celia; Forner, Stefania; Kawauchi, Shimako; Milinkeviciute, Giedre; Gomez-Arboledas, Angela; Neumann, Jonathan; Banh, Crystal E; Huynh, Michelle; Matheos, Dina P; Rezaie, Narges; Alcantara, Joshua A; Mortazavi, Ali; Wood, Marcelo A; Tenner, Andrea J; MacGregor, Grant R; Green, Kim N; LaFerla, Frank M.
Afiliación
  • Javonillo DI; Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, Irvine, CA, United States.
  • Tran KM; Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, Irvine, CA, United States.
  • Phan J; Department of Neurobiology and Behavior, University of California, Irvine, Irvine, CA, United States.
  • Hingco E; Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, Irvine, CA, United States.
  • Kramár EA; Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, Irvine, CA, United States.
  • da Cunha C; Department of Neurobiology and Behavior, University of California, Irvine, Irvine, CA, United States.
  • Forner S; Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, Irvine, CA, United States.
  • Kawauchi S; Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, Irvine, CA, United States.
  • Milinkeviciute G; Transgenic Mouse Facility, University Laboratory Animal Resources, Office of Research, University of California, Irvine, Irvine, CA, United States.
  • Gomez-Arboledas A; Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, Irvine, CA, United States.
  • Neumann J; Department of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, CA, United States.
  • Banh CE; Transgenic Mouse Facility, University Laboratory Animal Resources, Office of Research, University of California, Irvine, Irvine, CA, United States.
  • Huynh M; Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, Irvine, CA, United States.
  • Matheos DP; Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, Irvine, CA, United States.
  • Rezaie N; Department of Neurobiology and Behavior, University of California, Irvine, Irvine, CA, United States.
  • Alcantara JA; Department of Developmental and Cell Biology, University of California, Irvine, Irvine, CA, United States.
  • Mortazavi A; Center for Complex Biological Systems, University of California, Irvine, Irvine, CA, United States.
  • Wood MA; Transgenic Mouse Facility, University Laboratory Animal Resources, Office of Research, University of California, Irvine, Irvine, CA, United States.
  • Tenner AJ; Department of Developmental and Cell Biology, University of California, Irvine, Irvine, CA, United States.
  • MacGregor GR; Center for Complex Biological Systems, University of California, Irvine, Irvine, CA, United States.
  • Green KN; Department of Neurobiology and Behavior, University of California, Irvine, Irvine, CA, United States.
  • LaFerla FM; Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, Irvine, CA, United States.
Front Neurosci ; 15: 785276, 2021.
Article en En | MEDLINE | ID: mdl-35140584
ABSTRACT
Animal models of disease are valuable resources for investigating pathogenic mechanisms and potential therapeutic interventions. However, for complex disorders such as Alzheimer's disease (AD), the generation and availability of innumerous distinct animal models present unique challenges to AD researchers and hinder the success of useful therapies. Here, we conducted an in-depth analysis of the 3xTg-AD mouse model of AD across its lifespan to better inform the field of the various pathologies that appear at specific ages, and comment on drift that has occurred in the development of pathology in this line since its development 20 years ago. This modern characterization of the 3xTg-AD model includes an assessment of impairments in long-term potentiation followed by quantification of amyloid beta (Aß) plaque burden and neurofibrillary tau tangles, biochemical levels of Aß and tau protein, and neuropathological markers such as gliosis and accumulation of dystrophic neurites. We also present a novel comparison of the 3xTg-AD model with the 5xFAD model using the same deep-phenotyping characterization pipeline and show plasma NfL is strongly driven by plaque burden. The results from these analyses are freely available via the AD Knowledge Portal (https//modeladexplorer.org/). Our work demonstrates the utility of a characterization pipeline that generates robust and standardized information relevant to investigating and comparing disease etiologies of current and future models of AD.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Idioma: En Revista: Front Neurosci Año: 2021 Tipo del documento: Article País de afiliación: Estados Unidos
Texto completo
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Idioma: En Revista: Front Neurosci Año: 2021 Tipo del documento: Article País de afiliación: Estados Unidos