ArticleNature medicine1999
Transgenic mice with Alzheimer presenilin 1 mutations show accelerated neurodegeneration without amyloid plaque formation.
Article in Nature medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 117 papers.
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Who cites it
117 citing papers in PubMed, 366 citations in OpenAlex.
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- Pathological Calcium Signaling in Traumatic Brain Injury and Alzheimer's Disease: From Acute Neuronal Injury to Chronic Neurodegeneration.International journal of molecular sciences · 2025Review
- Abnormal calcium activity and CREB phosphorylation are associated with motor memory impairment in presenilin-1 mutant knock-in mice.Cell calcium · 2025Article
- Early molecular events of autosomal-dominant Alzheimer's disease in marmosets with PSEN1 mutations.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Repercussion of Primary Nucleation Pathway: Dementia and Cognitive Impairment.Current aging science · 2024Review
- A familial Alzheimer's disease associated mutation in presenilin-1 mediates amyloid-beta independent cell specific neurodegeneration.PloS one · 2024Article
- Use and Reuse of Animal Behavioral, Molecular, and Biochemical Data in Alzheimer's Disease Research: Focus on 3Rs and Saving People's Tax Dollars.Journal of Alzheimer's disease reports · 2024Review
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- Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology.Acta neuropathologica communications · 2023Article
- Precocious emergence of cognitive and synaptic dysfunction in 3xTg-AD mice exposed prenatally to ethanol.Alcohol (Fayetteville, N.Y.) · 2023Article
- In-Depth Characterization of Endo-Lysosomal Aβ in Intact Neurons.Biosensors · 2022Article
- Patient-Derived Fibroblasts With Presenilin-1 Mutations, That Model Aspects of Alzheimer's Disease Pathology, Constitute a Potential Object for Early Diagnosis.Frontiers in aging neuroscience · 2022Article
- Rodent Models of Amyloid-Beta Feature of Alzheimer's Disease: Development and Potential Treatment Implications.Aging and disease · 2020Review
- Correlation between β-amyloid deposits revealed by BF-227-PET imaging and brain atrophy detected by voxel-based morphometry-MR imaging: a pilot study.Nuclear medicine communications · 2019Article
- FeMolecular neurobiology · 2019Article
- Acquired Expression of MutantThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Ambrosin, a potent NF-κβ inhibitor, ameliorates lipopolysaccharide induced memory impairment, comparison to curcumin.PloS one · 2019Article
- Introduction of pathogenic mutations into the mouse Psen1 gene by Base Editor and Target-AID.Nature communications · 2018Article
- Fighting the Cause of Alzheimer's and GNE Myopathy.Frontiers in neuroscience · 2018Review
- Article
57 more citing papers are in PubMed but not listed here.
Corrections and comments
- Expression of concern
Authors and funding
13 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Familial Alzheimer disease mutations of presenilin 1 (PS-1) enhance the generation of A beta1-42, indicating that PS-1 is involved in amyloidogenesis. However, PS-1 transgenic mice have failed to show amyloid plaques in their brains. Because PS-1 mutations facilitate apoptotic neuronal death in vitro, we did careful quantitative studies in PS-1 transgenic mice and found that neurodegeneration was significantly accelerated in mice older than 13 months (aged mice) with familial Alzheimer disease mutant PS-1, without amyloid plaque formation. However, there were significantly more neurons containing intracellularly deposited A beta42 in aged mutant transgenic mice. Our data indicate that the pathogenic role of the PS-1 mutation is upstream of the amyloid cascade.
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Registered trials
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.