ArticleJournal of Alzheimer's disease : JAD2018
Differences in Synaptic Dysfunction Between rTg4510 and APP/PS1 Mouse Models of Alzheimer's Disease.
Article in Journal of Alzheimer's disease : JAD, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Article
- Cannabidiolic Acid Rescues Deficits in Hippocampal Long-Term Potentiation in Models of Alzheimer's Disease: An Electrophysiological and Proteomic Analysis.International journal of molecular sciences · 2025Article
- Navigating Alzheimer's Disease Mouse Models: Age-Related Pathology and Cognitive Deficits.Biomolecules · 2024Review
- A combination of ΔNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- Updates on mouse models of Alzheimer's disease.Molecular neurodegeneration · 2024Review
- Long-term potentiation-based screening identifies neuronal PYGM as a synaptic plasticity regulator participating in Alzheimer's disease.Zoological research · 2023Article
- Multiomics Analyses Identify Proline Endopeptidase-Like Protein As a Key Regulator of Protein Trafficking, a Pathway Underlying Alzheimer's Disease Pathogenesis.Molecular pharmacology · 2023Article
- Selective dysfunction of fast-spiking inhibitory interneurons and disruption of perineuronal nets in a tauopathy mouse model.iScience · 2023Article
- Alzheimer's disease as a synaptopathy: Evidence for dysfunction of synapses during disease progression.Frontiers in synaptic neuroscience · 2023Review
- The hibernation-derived compound SUL-138 shifts the mitochondrial proteome towards fatty acid metabolism and prevents cognitive decline and amyloid plaque formation in an Alzheimer's disease mouse model.Alzheimer's research & therapy · 2022Article
- The MK2 cascade mediates transient alteration in mGluR-LTD and spatial learning in a murine model of Alzheimer's disease.Aging cell · 2022Article
- Early Changes in Transcriptomic Profiles in Synaptodendrosomes Reveal Aberrant Synaptic Functions in Alzheimer's Disease.International journal of molecular sciences · 2022Article
- Plasticity in visual cortex is disrupted in a mouse model of tauopathy.Communications biology · 2022Article
- Torpor enhances synaptic strength and restores memory performance in a mouse model of Alzheimer's disease.Scientific reports · 2021Article
- FKBP52 overexpression accelerates hippocampal-dependent memory impairments in a tau transgenic mouse model.NPJ aging and mechanisms of disease · 2021Article
- Cornel Iridoid Glycoside Protects Against STAT1-Dependent Synapse and Memory Deficits by IncreasingFrontiers in aging neuroscience · 2021Article
- Acetylation of AMPA Receptors Regulates Receptor Trafficking and Rescues Memory Deficits in Alzheimer's Disease.iScience · 2020Article
- Cognitive Function Improvement in Mouse Model of Alzheimer's Disease Following Transcranial Direct Current Stimulation.Brain sciences · 2020Article
- Increasing cerebral blood flow improves cognition into late stages in Alzheimer's disease mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- AVP(4-8) Improves Cognitive Behaviors and Hippocampal Synaptic Plasticity in the APP/PS1 Mouse Model of Alzheimer's Disease.Neuroscience bulletin · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Genetically modified mice have provided insights into the progression and pathology of Alzheimer's disease (AD). Here, we have examined two mouse models of AD: the rTg4510 mouse, which overexpresses mutant human Tau gene, and the APP/PS1 mouse, which overexpresses mutant human genes for amyloid precursor protein and presenilin 1. Both models exhibit deficits in hippocampal function, but comparative analyses of these deficits are sparse. We used extracellular field potential recordings in hippocampal slices to study basal synaptic transmission (BST), paired-pulse facilitation (PPF), and long-term potentiation (LTP) at the Schaffer collateral-CA1 pyramidal cell synapses in both models. We found that 6-7, but not 2-3-month-old rTg4510 mice exhibited reduced pre-synaptic activation (fiber volley (FV) amplitude, ∼50%) and field excitatory post-synaptic potential (fEPSP) slope (∼40%) compared to wild-type controls. In contrast to previous reports, BST, when controlled for FV amplitude, was not altered in rTg4510. APP/PS1 mice (2-3 mo and 8-10 mo) had unchanged FV amplitude compared to wild-type controls, while fEPSP slope was reduced by ∼34% in older mice, indicating a deficit in BST. PPF was unchanged in 8-10-month-old APP/PS1 mice, but was reduced in 6-7-month-old rTg4510 mice. LTP was reduced only in older rTg4510 and APP/PS1 mice. Our data suggest that BST deficits appear earlier in APP/PS1 than in rTg4510, which exhibited no BST deficits at the ages tested. However, FV and synaptic plasticity deficits developed earlier in rTg4510. These findings highlight fundamental differences in the progression of synaptic pathology in two genetically distinct models of AD.
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