Cited by 583Alzheimer's disease research and treatmentsNeurological Disease Mechanisms and TreatmentsAmyotrophic Lateral Sclerosis Research

Animal models of neurodegenerative diseases

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Dawson, Ted M., Golde, Todd E., Lagier-Tourenne, Clotilde·2018·Nature Neuroscience

Abstract

Animal models of adult-onset neurodegenerative diseases have enhanced the understanding of the molecular pathogenesis of Alzheimer's disease, Parkinson's disease, frontotemporal dementia, and amyotrophic lateral sclerosis. Nevertheless, our understanding of these disorders and the development of mechanistically designed therapeutics can still benefit from more rigorous use of the models and from generation of animals that more faithfully recapitulate human disease. Here we review the current state of rodent models for Alzheimer's disease, Parkinson's disease, frontotemporal dementia, and amyotrophic lateral sclerosis. We discuss the limitations and utility of current models, issues regarding translatability, and future directions for developing animal models of these human disorders.

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Crossref · 10.1038/s41593-018-0236-8

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  • It typically requires additional expression of human tau harboring mutations associated with primary tauopathy or seeding mutant human APP knock-in mouse brain with human AD brain-derived tau to develop tau pathology in mouse models.

    “It typically requires additional expression of human tau harboring mutations associated with primary tauopathy (94–96) or seeding mutant human APP knock-in mouse brain with human AD brain-derived tau (97) to develop the tau pathology.”

    From Modeling late-onset Alzheimer’s disease neuropathology via direct neuronal reprogramming (2024) · cites this paper as [94]

    The sections on genetic-based tau and amyloid models (page not provided) say that mice overexpressing human tau with FTD-linked mutations develop tau pathology, while amyloid models generally lack prominent tau accumulation unless seeded with AD tau. The copy does not specify that the seeded mice are mutant human APP knock-in mice or that the tau is derived from human AD brain. (LLM, conf=0.85)

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  1. [111]Prusiner SB Prions. Proc Natl Acad Sci U S A 95, 13363– 13383 (1998). 9811807 PMC33918

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Authors
Dawson, T. M., Golde, T. E., & Lagier-Tourenne, C.
Affiliations
  • Johns Hopkins University (US)
  • University of Florida (US)
Corresponding author
  • Dawson, Ted M.
  • Golde, Todd E.
Venue
Nature Neuroscience
Published
2018-09-24
Volume
21
Issue
10
Pages
1370-1379
ISSN
  • 1097-6256 (ISSN-L)
  • 1546-1726
OpenAlex
W2891411797
Cited by
576
References
151
Citations by year
2026: 59 · 2025: 73 · 2024: 89 · 2023: 72 · 2022: 88 · 2021: 79 · 2020: 70 · 2019: 41 · 2018: 4
FWCI
6.37
Type
journal article
Language
en
Open access
Locations
  • Nature Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute on Aging (R01AG018454, U01AG046139, P50AG047266)
  • National Cancer Institute (P01CA166009)
  • National Institute of Neurological Disorders and Stroke (R21NS098006, R01NS087227, R01NS082205, P50NS038377)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
  • Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
Keywords
animal models, neurodegenerative diseases, Alzheimer's disease, Parkinson's disease, frontotemporal dementia, amyotrophic lateral sclerosis, rodent models, translatability, disease modeling
MeSH terms
Animals, Disease Models, Animal, Humans, Neurodegenerative Diseases

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