ArticlePloS one2015
DBA/2J genetic background exacerbates spontaneous lethal seizures but lessens amyloid deposition in a mouse model of Alzheimer's disease.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Mitochondrial-Targeted HDAP2 Preserves Retinal Ganglion Cells and Increases Pressure Tolerance in DBA/2J Mice.Investigative ophthalmology & visual science · 2025Article
- Mitochondrial-Targeted HDAP2 Preserves Retinal Ganglion Cells and Increases Pressure Tolerance in DBA/2J Mice.bioRxiv : the preprint server for biology · 2025Article
- Article
- Neocortical cholinergic pathology after neonatal brain injury is increased by Alzheimer's disease-related genes in mice.Neurobiology of disease · 2024Article
- Genetic diversity promotes resilience in a mouse model of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Genetically modified mice as a tool for the study of human diseases.Molecular biology reports · 2024Review
- The intracerebral injection of AβFrontiers in aging neuroscience · 2023Article
- Reduced excitatory neuron activity and interneuron-type-specific deficits in a mouse model of Alzheimer's disease.Communications biology · 2022Article
- Translational approaches to understanding resilience to Alzheimer's disease.Trends in neurosciences · 2022Review
- Inbred Mice Again at Stake: How the Cognitive Profile of the Wild-Type Mouse Background Discloses Pathogenic Effects of APP Mutations.Frontiers in behavioral neuroscience · 2022Review
- The Contribution of Anterior Segment Abnormalities to Changes in Intraocular Pressure in the DBA/2J Mouse Model of Glaucoma: DBA/2J-Frontiers in neuroscience · 2021Article
- Regulation of intrinsic excitability: Roles for learning and memory, aging and Alzheimer's disease, and genetic diversity.Neurobiology of learning and memory · 2019Review
- Enhancing face validity of mouse models of Alzheimer's disease with natural genetic variation.PLoS genetics · 2019Article
- Article
- Review
- Transgenic Mouse Models as Tools for Understanding How Increased Cognitive and Physical Stimulation Can Improve Cognition in Alzheimer's Disease.Brain plasticity (Amsterdam, Netherlands) · 2018Review
- Altered glutamate clearance in ascorbate deficient mice increases seizure susceptibility and contributes to cognitive impairment in APP/PSEN1 mice.Neurobiology of aging · 2018Article
- Integrated analysis of human genetic association study and mouse transcriptome suggests LBH and SHF genes as novel susceptible genes for amyloid-β accumulation in Alzheimer's disease.Human genetics · 2018Article
- Practical considerations for choosing a mouse model of Alzheimer's disease.Molecular neurodegeneration · 2017Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Alzheimer's disease (AD) is a leading cause of dementia in the elderly and is characterized by amyloid plaques, neurofibrillary tangles (NFTs) and neuronal dysfunction. Early onset AD (EOAD) is commonly caused by mutations in amyloid precursor protein (APP) or genes involved in the processing of APP including the presenilins (e.g. PSEN1 or PSEN2). In general, mouse models relevant to EOAD recapitulate amyloidosis, show only limited amounts of NFTs and neuronal cell dysfunction and low but significant levels of seizure susceptibility. To investigate the effect of genetic background on these phenotypes, we generated APPswe and PSEN1de9 transgenic mice on the seizure prone inbred strain background, DBA/2J. Previous studies show that the DBA/2J genetic background modifies plaque deposition in the presence of mutant APP but the impact of PSEN1de9 has not been tested. Our study shows that DBA/2J.APPswePSEN1de9 mice are significantly more prone to premature lethality, likely to due to lethal seizures, compared to B6.APPswePSEN1de9 mice-70% of DBA/2J.APPswePSEN1de9 mice die between 2-3 months of age. Of the DBA/2J.APPswePSEN1de9 mice that survived to 6 months of age, plaque deposition was greatly reduced compared to age-matched B6.APPswePSEN1de9 mice. The reduction in plaque deposition appears to be independent of microglia numbers, reactive astrocytosis and complement C5 activity.
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