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Tytuł pozycji:

Alzheimer's Disease Animal Models: Elucidation of Biomarkers and Therapeutic Approaches for Cognitive Impairment.

Tytuł:
Alzheimer's Disease Animal Models: Elucidation of Biomarkers and Therapeutic Approaches for Cognitive Impairment.
Autorzy:
Nakai T; Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya 466-8560, Japan.
Yamada K; Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya 466-8560, Japan.
Mizoguchi H; Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya 466-8560, Japan.; Medical Interactive Research and Academia Industry Collaboration Center, Research Institute of Environmental Medicine, Nagoya University, Nagoya 464-8601, Japan.
Źródło:
International journal of molecular sciences [Int J Mol Sci] 2021 May 24; Vol. 22 (11). Date of Electronic Publication: 2021 May 24.
Typ publikacji:
Journal Article; Review
Język:
English
Imprint Name(s):
Original Publication: Basel, Switzerland : MDPI, [2000-
MeSH Terms:
Disease Models, Animal*
Alzheimer Disease/*drug therapy
Alzheimer Disease/*metabolism
Amyloid beta-Protein Precursor/*metabolism
Cognitive Dysfunction/*metabolism
tau Proteins/*metabolism
Alzheimer Disease/pathology ; Amyloid beta-Protein Precursor/genetics ; Animals ; Biomarkers/metabolism ; Cognitive Dysfunction/pathology ; Gene Knock-In Techniques ; Mice ; Mice, Transgenic
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Grant Information:
19H03532, 19H05017, 19K21811, 20H01037 Grants-in-Aid for Scientific Research from MEXT; non biomedical research from the SRF, Japan; non the Takeda Science Foundation; non the Mishima Kaiun Memorial Foundation; non the Hori Sciences and Arts Foundation; non the Strategic Research Program for Brain Science from the Japan Agency for Medical Research and Development (AMED)
Contributed Indexing:
Keywords: Alzheimer’s disease; amyloid cascade hypothesis; animal models; biomarkers; neurofibrillary tangles; pharmacological intervention; tau
Substance Nomenclature:
0 (Amyloid beta-Protein Precursor)
0 (Biomarkers)
0 (tau Proteins)
Entry Date(s):
Date Created: 20210602 Date Completed: 20210624 Latest Revision: 20210624
Update Code:
20240104
PubMed Central ID:
PMC8197360
DOI:
10.3390/ijms22115549
PMID:
34074018
Czasopismo naukowe
Alzheimer's disease (AD) is an age-related and progressive neurodegenerative disorder. It is widely accepted that AD is mainly caused by the accumulation of extracellular amyloid β (Aβ) and intracellular neurofibrillary tau tangles. Aβ begins to accumulate years before the onset of cognitive impairment, suggesting that the benefit of currently available interventions would be greater if they were initiated in the early phases of AD. To understand the mechanisms of AD pathogenesis, various transgenic mouse models with an accelerated accumulation of Aβ and tau tangles have been developed. However, none of these models exhibit all pathologies present in human AD. To overcome these undesirable phenotypes, APP knock-in mice, which were presented with touchscreen-based tasks, were developed to better evaluate the efficacy of candidate therapeutics in mouse models of early-stage AD. This review assesses several AD mouse models from the aspect of biomarkers and cognitive impairment and discusses their potential as tools to provide novel AD therapeutic approaches.
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