ArticleThe Journal of comparative neurology2014
Early fear memory defects are associated with altered synaptic plasticity and molecular architecture in the TgCRND8 Alzheimer's disease mouse model.
Article in The Journal of comparative neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 47 citations in OpenAlex.
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- Genetic and pharmacologic enhancement of SUMO2 conjugation prevents and reverses cognitive impairment and synaptotoxicity in a preclinical model of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Structural plasticity of pyramidal cell neurons measured after FLASH and conventional dose-rate irradiation.Brain structure & function · 2025Article
- Enhanced prefrontal nicotinic signaling as evidence of active compensation in Alzheimer's disease models.Translational neurodegeneration · 2024Article
- Navigating Alzheimer's Disease Mouse Models: Age-Related Pathology and Cognitive Deficits.Biomolecules · 2024Review
- Structural plasticity of pyramidal cell neurons measured after FLASH and conventional dose-rate irradiation.Research square · 2024Article
- Maf1 loss regulates spinogenesis and attenuates cognitive impairment in Alzheimer's disease.Brain : a journal of neurology · 2024Article
- Control of hippocampal synaptic plasticity by microglia-dendrite interactions depends on genetic context in mouse models of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Genetic context controls early microglia-synaptic interactions in mouse models of Alzheimer's disease.bioRxiv : the preprint server for biology · 2023Article
- The intracellular domain of major histocompatibility class-I proteins is essential for maintaining excitatory spine density and synaptic ultrastructure in the brain.Scientific reports · 2023Article
- Progressive sleep disturbance in various transgenic mouse models of Alzheimer's disease.Frontiers in aging neuroscience · 2023Review
- Ultrasound delivery of a TrkA agonist confers neuroprotection to Alzheimer-associated pathologies.Brain : a journal of neurology · 2022Article
- Structural Plasticity of the Hippocampus in Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Regulation of Melatonin and Neurotransmission in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Chronic Low Dose Neutron Exposure Results in Altered Neurotransmission Properties of the Hippocampus-Prefrontal Cortex Axis in Both Mice and Rats.International journal of molecular sciences · 2021Article
- FMRP regulates the subcellular distribution of cortical dendritic spine density in a non-cell-autonomous manner.Neurobiology of disease · 2021Article
- Suan-Zao-Ren Decoction ameliorates synaptic plasticity through inhibition of the Aβ deposition and JAK2/STAT3 signaling pathway in AD model of APP/PS1 transgenic mice.Chinese medicine · 2021Article
- Tau is not necessary for amyloid-β-induced synaptic and memory impairments.The Journal of clinical investigation · 2020Article
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Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
Abstract
Alzheimer's disease (AD) is a complex and slowly progressing dementing disorder that results in neuronal and synaptic loss, deposition in brain of aberrantly folded proteins, and impairment of spatial and episodic memory. Most studies of mouse models of AD have employed analyses of cognitive status and assessment of amyloid burden, gliosis, and molecular pathology during disease progression. Here we sought to understand the behavioral, cellular, ultrastructural, and molecular changes that occur at a pathological stage equivalent to the early stages of human AD. We studied the TgCRND8 mouse, a model of aggressive AD amyloidosis, at an early stage of plaque pathology (3 months of age) in comparison to their wildtype littermates and assessed changes in cognition, neuron and spine structure, and expression of synaptic glutamate receptor proteins. We found that, at this age, TgCRND8 mice display substantial plaque deposition in the neocortex and hippocampus and impairment on cued and contextual memory tasks. Of particular interest, we also observed a significant decrease in the number of neurons in the hippocampus. Furthermore, analysis of CA1 neurons revealed significant changes in apical and basal dendritic spine types, as well as altered expression of GluN1 and GluA2 receptors. This change in molecular architecture within the hippocampus may reflect a rising representation of inherently less stable thin spine populations, which can cause cognitive decline. These changes, taken together with toxic insults from amyloid-β protein, may underlie the observed neuronal loss.
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