ArticleNeuroscience bulletin2014
Intraneuronal accumulation of Aβ42 induces age-dependent slowing of neuronal transmission in Drosophila.
Article in Neuroscience bulletin, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed.
- Conditioned Generative Modeling of Molecular Glues: A Realistic AI Approach for Synthesizable Drug-like Molecules.Biomolecules · 2025Article
- Experimental modeling of Alzheimer's disease: Translational lessons from cross-taxon analyses.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Single-cell type analysis of wing premotor circuits in the ventral nerve cord ofbioRxiv : the preprint server for biology · 2025Article
- PI3K activation prevents Aβ42-induced synapse loss and favors insoluble amyloid deposit formation.Molecular biology of the cell · 2020Article
- Article
- Downregulation of RBO-PI4KIIIα Facilitates AβThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Modeling the complex pathology of Alzheimer's disease in Drosophila.Experimental neurology · 2015Review
- Automated rapid iterative negative geotaxis assay and its use in a genetic screen for modifiers of Aβ(42)-induced locomotor decline in Drosophila.Neuroscience bulletin · 2015Article
- Alzheimer's disease: from molecule to clinic.Neuroscience bulletin · 2014Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Beta amyloid (Aβ42)-induced dysfunction and loss of synapses are believed to be major underlying mechanisms for the progressive loss of learning and memory abilities in Alzheimer's disease (AD). The vast majority of investigations on AD-related synaptic impairment focus on synaptic plasticity, especially the decline of long-term potentiation of synaptic transmission caused by extracellular Aβ42. Changes in other aspects of synaptic and neuronal functions are less studied or undiscovered. Here, we report that intraneuronal accumulation of Aβ42 induced an age-dependent slowing of neuronal transmission along pathways involving multiple synapses.
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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 OpenQuestion graph.