ArticleMolecular neurodegeneration2020
Contribution of GABAergic interneurons to amyloid-β plaque pathology in an APP knock-in mouse model.
Article in Molecular neurodegeneration, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- A Question of Origins: Non-neuronal Sources of Amyloid-β.Neuroscience bulletin · 2026Review
- Selective weakening of population-coupled synaptic activity in vivo in a mouse model of amyloid-beta pathology.Nature communications · 2026Article
- A compound pulsed magnetic field achieves superior cognitive benefits against Alzheimer's disease progression via multi-level restoration of neural oscillations and cerebral perfusion.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Neuronal subtype governs amyloid structure, cellular response, and cognitive outcome in genetically targeted APP mouse models.Molecular neurodegeneration · 2026Article
- Identification ofFrontiers in aging neuroscience · 2026Article
- Progressive changes in synapses and glial cells inBrain communications · 2026Article
- Circadian rhythms and the light-dark cycle interact to regulate amyloid-beta plaque accumulation and tau phosphorylation in 5xFAD mice.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Characterization of adult hippocampal neurogenesis in the novelbioRxiv : the preprint server for biology · 2025Article
- Experimental modeling of Alzheimer's disease: Translational lessons from cross-taxon analyses.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Alzheimer's Disease-Derived Outer Membrane Vesicles Exacerbate Cognitive Dysfunction, Modulate the Gut Microbiome, and Increase Neuroinflammation and Amyloid-β Production.Molecular neurobiology · 2025Article
- Neural circuit mechanisms underlying aberrantly prolonged functional hyperemia in young Alzheimer's disease mice.Molecular psychiatry · 2025Article
- Quantification and correlation of amyloid-β plaque load, glial activation, GABAergic interneuron numbers, and cognitive decline in the young TgF344-AD rat model of Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- Article
- Oligodendrocytes produce amyloid-β and contribute to plaque formation alongside neurons in Alzheimer's disease model mice.Nature neuroscience · 2024Article
- Fast-spiking parvalbumin-positive interneurons in brain physiology and Alzheimer's disease.Molecular psychiatry · 2023Review
- Physiological Roles of β-amyloid in Regulating Synaptic Function: Implications for AD Pathophysiology.Neuroscience bulletin · 2023Review
- Helicobacter pylori-derived outer membrane vesicles contribute to Alzheimer's disease pathogenesis via C3-C3aR signalling.Journal of extracellular vesicles · 2023Article
- Early Life Stress Enhances Cognitive Decline and Alters Synapse Function and Interneuron Numbers in Young Male APP/PS1 Mice.Journal of Alzheimer's disease : JAD · 2023Article
- Local and long-range GABAergic circuits in hippocampal area CA1 and their link to Alzheimer's disease.Frontiers in neural circuits · 2023Review
- MDGA1 negatively regulates amyloid precursor protein-mediated synapse inhibition in the hippocampus.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 5 countries.
Funding
Abstract
The amyloid-β (Aβ) peptide, the primary constituent of amyloid plaques found in Alzheimer's disease (AD) brains, is derived from sequential proteolytic processing of the Amyloid Precursor Protein (APP). However, the contribution of different cell types to Aβ deposition has not yet been examined in an in vivo, non-overexpression system. Here, we show that endogenous APP is highly expressed in a heterogeneous subset of GABAergic interneurons throughout various laminae of the hippocampus, suggesting that these cells may have a profound contribution to AD plaque pathology. We then characterized the laminar distribution of amyloid burden in the hippocampus of an APP knock-in mouse model of AD. To examine the contribution of GABAergic interneurons to plaque pathology, we blocked Aβ production specifically in these cells using a cell type-specific knock-out of BACE1. We found that during early stages of plaque deposition, interneurons contribute to approximately 30% of the total plaque load in the hippocampus. The greatest contribution to plaque load (75%) occurs in the stratum pyramidale of CA1, where plaques in human AD cases are most prevalent and where pyramidal cell bodies and synaptic boutons from perisomatic-targeting interneurons are located. These findings reveal a crucial role of GABAergic interneurons in the pathology of AD. Our study also highlights the necessity of using APP knock-in models to correctly evaluate the cellular contribution to amyloid burden since APP overexpressing transgenic models drive expression in cell types according to the promoter and integration site and not according to physiologically relevant expression mechanisms.
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