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Cited by 114Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Insights into Alzheimer disease pathogenesis from studies in transgenic animal models

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Schaeffer, Evelin L, Figueiró, Micheli, Gattaz, Wagner F·2011·Clinics
DOI 10.1590/s1807-59322011001300006PMC PMC3118437
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Abstract

Alzheimer disease is the most common cause of dementia among the elderly, accounting for ~60-70% of all cases of dementia. The neuropathological hallmarks of Alzheimer disease are senile plaques (mainly containing p-amyloid peptide derived from amyloid precursor protein) and neurofibrillary tangles (containing hyperphosphorylated Tau protein), along with neuronal loss. At present there is no effective treatment for Alzheimer disease. Given the prevalence and poor prognosis of the disease, the development of animal models has been a research priority to understand pathogenic mechanisms and to test therapeutic strategies. Most cases of Alzheimer disease occur sporadically in people over 65 years old, and are not genetically inherited. Roughly 5% of patients with Alzheimer disease have familial Alzheimer disease--that is, related to a genetic predisposition, including mutations in the amyloid precursor protein, presenilin 1, and presenilin 2 genes. The discovery of genes for familial Alzheimer disease has allowed transgenic models to be generated through the overexpression of the amyloid precursor protein and/or presenilins harboring one or several mutations found in familial Alzheimer disease. Although none of these models fully replicates the human disease, they have provided valuable insights into disease mechanisms as well as opportunities to test therapeutic approaches. This review describes the main transgenic mouse models of Alzheimer disease which have been adopted in Alzheimer disease research, and discusses the insights into Alzheimer disease pathogenesis from studies in such models. In summary, the Alzheimer disease mouse models have been the key to understanding the roles of soluble b-amyloid oligomers in disease pathogenesis, as well as of the relationship between p-amyloid and Tau pathologies.

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  • The increased baseline KYN in Tg2576 mice is likely due to a heightened baseline level of inflammatory cytokines in Tg2576 mice.

    “This is likely due to the heightened baseline level of inflammatory cytokines in Tg2576 mice, given that these mice are predisposed to acquire amyloid beta tangles and AD neuropathology [45].”

    From VEEV TC-83 Triggers Dysregulation of the Tryptophan–Kynurenine Pathway in the Central Nervous System That Correlates with Cognitive Impairment in Tg2576 Mice (2024) · cites this paper as [45]

    Section 2 (page not supplied) reports that Tg2576 mice develop age-dependent amyloid-β deposition, senile plaques, and associated gliosis, supporting the AD-neuropathology premise. It does not report elevated baseline inflammatory cytokines or KYN, or link the two; it describes amyloid-β plaques, not amyloid-β tangles. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • Tg2576 mice are predisposed to acquire amyloid beta tangles and AD neuropathology.

    “given that these mice are predisposed to acquire amyloid beta tangles and AD neuropathology [45].”

    From VEEV TC-83 Triggers Dysregulation of the Tryptophan–Kynurenine Pathway in the Central Nervous System That Correlates with Cognitive Impairment in Tg2576 Mice (2024) · cites this paper as [45]

    The 'Transgenic mouse models of Alzheimer disease' section reports that Tg2576 mice develop age-dependent Aβ deposition, senile plaques, and associated abnormalities. It does not say Tg2576 mice develop 'amyloid beta tangles': it describes neurofibrillary tangles in TAPP mice produced by crossing Tg2576 with a mutant-Tau line. No page numbers are provided in the supplied passages. (LLM, conf=0.88)

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Sorted by citations

Authors
Schaeffer, E. L., Figueiró, M., & Gattaz, W. F.
Affiliations
Universidade de São Paulo (BR)
ORCID
Gattaz, Wagner F
Venue
Clinics
Publisher
Elsevier BV
Published
2011-01
Volume
66
Pages
45-54
ISSN
1807-5932 (ISSN-L)
DOI
10.1590/s1807-59322011001300006
PMC
PMC3118437
OpenAlex
W2087011206
Cited by
114
References
112
Citations by year
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FWCI
1.39
Type
journal article
Language
en
Open access
Licence
Locations
  • Clinics (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (publishedVersion, other-oa)
  • Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (publishedVersion)
  • Americanae (AECID Library) (submittedVersion, other-oa)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Alzheimer's disease, transgenic mouse model, amyloid precursor protein, presenilin 1, presenilin 2, familial Alzheimer's disease, amyloid plaques, neurofibrillary tangles, tau hyperphosphorylation, soluble amyloid-beta oligomers, pathogenesis, therapeutic testing
MeSH terms
Alzheimer Disease, Animals, Disease Models, Animal, Humans, Mice, Transgenic, Mutation, Amyloid beta-Protein Precursor, Mice

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