ArticleiScience2024
Early hippocampal hyperexcitability and synaptic reorganization in mouse models of amyloidosis.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Presynaptic accumulation of APP-CTFβ may contribute to synaptic dysfunction in Alzheimer's disease.The EMBO journal · 2026Article
- [Noninvasive nanosecond transcranial pulsed electric fields: deep-penetrating, high-field stimulation for suppressing hippocampal amyloid-β and improving cognitive function in an Alzheimer's disease model].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2026Article
- Article
- Lamellar Normative Modelling of the Hippocampus Across the Human Lifespan.bioRxiv : the preprint server for biology · 2026Article
- Fucoxanthin attenuates carbonyl stress and neuroinflammation by modulating MGO/RAGE/NF-κB axis in Aβ-induced models.Frontiers in pharmacology · 2026Article
- Pre-plaque glutamatergic hyperexcitability, mitochondrial dysfunction, and dendritic remodeling in the hippocampus of one-month-old 5xFAD mice.Frontiers in aging neuroscience · 2026Article
- Evaluation of hippocampal DLGAP2 overexpression on cognition, synaptic function, and dendritic spine structure in a translationally relevant AD mouse model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Neuronal and Glial α7 Nicotinic Acetylcholine Receptors: Role in Alzheimer's Disease Pathophysiology.Life (Basel, Switzerland) · 2025Review
- The role of inhibitory immune checkpoint receptors in the pathogenesis of Alzheimer's disease.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Therapeutic and preventive strategies based on the maladaptive plasticity hypothesis for Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- The transcriptional and cellular landscape of cognitive resilience to Alzheimer's disease.Frontiers in molecular neuroscience · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
The limited success of plaque-reducing therapies in Alzheimer's disease suggests that early treatment might be more effective in delaying or reversing memory impairments. Toward this end, it is important to establish the progression of synaptic and circuit changes before onset of plaques or cognitive deficits. Here, we used quantitative, fluorescence-based methods for synapse detection in CA1 pyramidal neurons to investigate the interaction between abnormal circuit activity, measured by Fos-immunoreactivity, and synapse reorganization in mouse models of amyloidosis. Using a genetically encoded, fluorescently labeled synaptic marker in juvenile mice (prior to sexual maturity), we find both synapse gain and loss depending on dendritic location. This progresses to broad synapse loss in aged mice. Elevated hippocampal activity in both CA3 and CA1 was present at weaning and preceded this reorganization. Thus, Aβ overproduction may initiate abnormal activity and subsequent input-specific synapse plasticity. These findings indicate that sustained amyloidosis drives heterogeneous and progressive circuit-wide abnormalities.
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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 Socratic graph.