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APP mouse models for Alzheimer's disease preclinical studies.

Abstract Animal models of human diseases that accurately recapitulate clinical pathology are indispensable for understanding molecular mechanisms and advancing preclinical studies. The Alzheimer's disease (AD) research community has historically used first-generation transgenic (Tg) mouse models that overexpress proteins linked to familial AD (FAD), mutant amyloid precursor protein (APP), or APP and presenilin (PS). These mice exhibit AD pathology, but the overexpression paradigm may cause additional phenotypes unrelated to AD Second-generation mouse models contain humanized sequences and clinical mutations in the endogenous mouse App gene. These mice show Aβ accumulation without phenotypes related to overexpression but are not yet a clinical recapitulation of human AD In this review, we evaluate different APP mouse models of AD, and review recent studies using the second-generation mice. We advise AD researchers to consider the comparative strengths and limitations of each model against the scientific and therapeutic goal of a prospective preclinical study.
PMID
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Authors

Mayor MeshTerms
Keywords

APP transgenic

Alzheimer's disease

App knock‐in

amyloid precursor protein

amyloid β peptide

Journal Title the embo journal
Publication Year Start




PMID- 28768718
OWN - NLM
STAT- Publisher
DA  - 20170803
LR  - 20170803
IS  - 1460-2075 (Electronic)
IS  - 0261-4189 (Linking)
DP  - 2017 Aug 01
TI  - APP mouse models for Alzheimer's disease preclinical studies.
LID - e201797397 [pii]
LID - 10.15252/embj.201797397 [doi]
AB  - Animal models of human diseases that accurately recapitulate clinical pathology
      are indispensable for understanding molecular mechanisms and advancing
      preclinical studies. The Alzheimer's disease (AD) research community has
      historically used first-generation transgenic (Tg) mouse models that overexpress 
      proteins linked to familial AD (FAD), mutant amyloid precursor protein (APP), or 
      APP and presenilin (PS). These mice exhibit AD pathology, but the overexpression 
      paradigm may cause additional phenotypes unrelated to AD Second-generation mouse 
      models contain humanized sequences and clinical mutations in the endogenous mouse
      App gene. These mice show Abeta accumulation without phenotypes related to
      overexpression but are not yet a clinical recapitulation of human AD In this
      review, we evaluate different APP mouse models of AD, and review recent studies
      using the second-generation mice. We advise AD researchers to consider the
      comparative strengths and limitations of each model against the scientific and
      therapeutic goal of a prospective preclinical study.
CI  - (c) 2017 The Authors. Published under the terms of the CC BY 4.0 license.
FAU - Sasaguri, Hiroki
AU  - Sasaguri H
AUID- ORCID: http://orcid.org/0000-0003-2550-9156
AD  - Laboratory for Proteolytic Neuroscience, RIKEN Brain Science Institute, Wako,
      Japan [email protected] [email protected]
AD  - Department of Neurology and Neurological Science, Graduate School of Medicine,
      Tokyo Medical and Dental University, Tokyo, Japan.
FAU - Nilsson, Per
AU  - Nilsson P
AUID- ORCID: http://orcid.org/0000-0001-6450-0870
AD  - Laboratory for Proteolytic Neuroscience, RIKEN Brain Science Institute, Wako,
      Japan.
AD  - Division of Neurogeriatrics, Department of Neurobiology, Care Sciences and
      Society, Center for Alzheimer Research, Karolinska Institutet, Huddinge, Sweden.
FAU - Hashimoto, Shoko
AU  - Hashimoto S
AUID- ORCID: http://orcid.org/0000-0002-5778-4884
AD  - Laboratory for Proteolytic Neuroscience, RIKEN Brain Science Institute, Wako,
      Japan.
FAU - Nagata, Kenichi
AU  - Nagata K
AUID- ORCID: http://orcid.org/0000-0001-8377-7197
AD  - Laboratory for Proteolytic Neuroscience, RIKEN Brain Science Institute, Wako,
      Japan.
FAU - Saito, Takashi
AU  - Saito T
AUID- ORCID: http://orcid.org/0000-0002-9659-9251
AD  - Laboratory for Proteolytic Neuroscience, RIKEN Brain Science Institute, Wako,
      Japan.
AD  - Department of Neuroscience and Pathobiology, Research Institute of Environmental 
      Medicine, Nagoya University, Nagoya, Japan.
FAU - De Strooper, Bart
AU  - De Strooper B
AUID- ORCID: http://orcid.org/0000-0001-5455-5819
AD  - Dementia Research Institute, University College London, London, UK.
AD  - Department for Neurosciences, KU Leuven, Leuven, Belgium.
AD  - VIB Center for Brain and Disease Research, Leuven, Belgium.
FAU - Hardy, John
AU  - Hardy J
AUID- ORCID: http://orcid.org/0000-0002-3122-0423
AD  - Reta Lila Research Laboratories and the Department of Molecular Neuroscience,
      University College London Institute of Neurology, London, UK.
FAU - Vassar, Robert
AU  - Vassar R
AD  - Department of Cell and Molecular Biology, Feinberg School of Medicine,
      Northwestern University, Chicago, IL, USA.
FAU - Winblad, Bengt
AU  - Winblad B
AUID- ORCID: http://orcid.org/0000-0002-0011-1179
AD  - Division of Neurogeriatrics, Department of Neurobiology, Care Sciences and
      Society, Center for Alzheimer Research, Karolinska Institutet, Huddinge, Sweden.
FAU - Saido, Takaomi C
AU  - Saido TC
AUID- ORCID: http://orcid.org/0000-0003-1970-6903
AD  - Laboratory for Proteolytic Neuroscience, RIKEN Brain Science Institute, Wako,
      Japan [email protected] [email protected]
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170801
PL  - England
TA  - EMBO J
JT  - The EMBO journal
JID - 8208664
OTO - NOTNLM
OT  - APP transgenic
OT  - Alzheimer's disease
OT  - App knock-in
OT  - amyloid precursor protein
OT  - amyloid beta peptide
EDAT- 2017/08/05 06:00
MHDA- 2017/08/05 06:00
CRDT- 2017/08/04 06:00
PHST- 2017/05/19 [received]
PHST- 2017/06/09 [revised]
PHST- 2017/07/07 [accepted]
AID - embj.201797397 [pii]
AID - 10.15252/embj.201797397 [doi]
PST - aheadofprint
SO  - EMBO J. 2017 Aug 1. pii: e201797397. doi: 10.15252/embj.201797397.