ArticleThe American journal of pathology2000
Age-related amyloid beta deposition in transgenic mice overexpressing both Alzheimer mutant presenilin 1 and amyloid beta precursor protein Swedish mutant is not associated with global neuronal loss.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 91 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
91 citing papers in PubMed, 228 citations in OpenAlex.
- Ceramides may Play a Central Role in the Pathogenesis of Alzheimer's Disease: a Review of Evidence and Horizons for Discovery.Molecular neurobiology · 2025Review
- The autocrine motility factor receptor delays the pathological progression of Alzheimer's disease via regulating the ubiquitination-mediated degradation of APP.Alzheimer's research & therapy · 2025Article
- Evolution of Alzheimer's Disease Therapeutics: From Conventional Drugs to Medicinal Plants, Immunotherapy, Microbiotherapy and Nanotherapy.Pharmaceutics · 2025Review
- Increased expression of the proapoptotic presenilin associated protein is involved in neuronal tangle formation in human brain.Scientific reports · 2024Article
- Updates on mouse models of Alzheimer's disease.Molecular neurodegeneration · 2024Review
- Insights on the Use of Transgenic Mice Models in Alzheimer's Disease Research.International journal of molecular sciences · 2024Review
- The past and present of therapeutic strategy for Alzheimer's diseases: potential for stem cell therapy.Experimental animals · 2023Review
- Aducanumab-Hope or Disappointment for Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Histone Deacetylase 2 Knockdown Ameliorates Morphological Abnormalities of Dendritic Branches and Spines to Improve Synaptic Plasticity in an APP/PS1 Transgenic Mouse Model.Frontiers in molecular neuroscience · 2021Article
- Liver Growth Factor "LGF" as a Therapeutic Agent for Alzheimer's Disease.International journal of molecular sciences · 2020Article
- Phosphorylated Aβ peptides in human Down syndrome brain and different Alzheimer's-like mouse models.Acta neuropathologica communications · 2020Article
- Microglial Activation in the Retina of a Triple-Transgenic Alzheimer's Disease Mouse Model (3xTg-AD).International journal of molecular sciences · 2020Article
- Urolithin A attenuates memory impairment and neuroinflammation in APP/PS1 mice.Journal of neuroinflammation · 2019Article
- Genome analysis of Yucatan miniature pigs to assess their potential as biomedical model animals.Asian-Australasian journal of animal sciences · 2019Article
- High-fat diet worsens the impact of aging on microglial function and morphology in a region-specific manner.Neurobiology of aging · 2019Article
- Can Animal Models Inform on the Relationship between Depression and Alzheimer Disease?Canadian journal of psychiatry. Revue canadienne de psychiatrie · 2019Review
- Genetically engineered pigs as models for human disease.Disease models & mechanisms · 2018Review
- Alzheimer's disease: experimental models and reality.Acta neuropathologica · 2017Review
- Progranulin gene delivery reduces plaque burden and synaptic atrophy in a mouse model of Alzheimer's disease.PloS one · 2017Article
- The Role of Microglia in Retinal Neurodegeneration: Alzheimer's Disease, Parkinson, and Glaucoma.Frontiers in aging neuroscience · 2017Review
31 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 6 institutions in 3 countries.
Funding
Abstract
To analyze the relationship between the deposition of amyloid beta peptides (Abeta) and neuronal loss in transgenic models of Alzheimer's disease (AD), we examined the frontal neocortex (Fc) and CA1 portion of hippocampus (CA1) in PSAPP mice doubly expressing AD-associated mutant presenilin 1 (PS1) and Swedish-type mutant beta amyloid precursor protein (APPsw) by morphometry of Abeta burden and neuronal counts. Deposition of Abeta was detected as early as 3 months of age in the Fc and CA1 of PSAPP mice and progressed to cover 28.3% of the superior frontal cortex and 18.4% of CA1 at 12 months: approximately 20- (Fc) and approximately 40- (CA1) fold greater deposition than in APPsw mice. There was no significant difference in neuronal counts in either CA1 or the frontal cortex between nontransgenic (non-tg), PS1 transgenic, APPsw, and PSAPP mice at 3 to 12 months of age. In the PSAPP mice, there was disorganization of the neuronal architecture by compact amyloid plaques, and the average number of neurons was 8 to 10% fewer than the other groups (NS, P > 0.10) in CA1 and 2 to 20% fewer in frontal cortex (NS, P = 0.31). There was no loss of total synaptophysin immunoreactivity in the Fc or dentate gyrus molecular layer of the 12-month-old PSAPP mice. Thus, although co-expression of mutant PS1 with Swedish mutant betaAPP leads to marked cortical and limbic Abeta deposition in an age-dependent manner, it does not result in the dramatic neuronal loss in hippocampus and association cortex characteristic of AD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.