ArticleACS chemical neuroscience2018
Physiological Aβ Concentrations Produce a More Biomimetic Representation of the Alzheimer's Disease Phenotype in iPSC Derived Human Neurons.
Article in ACS chemical neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Composition and activity of the proteasome in human iPSC-derived neuronal model of early-stage sporadic Alzheimer's disease.bioRxiv : the preprint server for biology · 2026Article
- A Model for the Development of Alzheimer's Disease.Genomics, proteomics & bioinformatics · 2025Article
- Divergent actions of physiological and pathological amyloid-β on synapses in live human brain slice cultures.Nature communications · 2025Article
- Organelle perturbation in Alzheimer's disease: do intracellular amyloid-ß and the fragmented Golgi mediate early intracellular neurotoxicity?Frontiers in cell and developmental biology · 2025Review
- Construction of a Dataset for All Expressed Transcripts for Alzheimer's Disease Research.Brain sciences · 2024Article
- Validation of a functional human AD model with four AD therapeutics utilizing patterned ipsc-derived cortical neurons integrated with microelectrode arrays.Scientific reports · 2024Article
- A functional aged human iPSC-cortical neuron model recapitulates Alzheimer's disease, senescence, and the response to therapeutics.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Validation of a functional human AD model with four AD therapeutics utilizing patterned iPSC-derived cortical neurons integrated with microelectrode arrays.Research square · 2024Article
- Seeing Neurodegeneration in a New Light Using Genetically Encoded Fluorescent Biosensors and iPSCs.International journal of molecular sciences · 2023Review
- The intracerebral injection of AβFrontiers in aging neuroscience · 2023Article
- Amyloid-β42/40 ratio drives tau pathology in 3D human neural cell culture models of Alzheimer's disease.Nature communications · 2020Article
- Modeling Alzheimer's disease with iPSC-derived brain cells.Molecular psychiatry · 2020Review
- A human induced pluripotent stem cell-derived cortical neuron human-on-a chip system to study AβAlzheimer's & dementia (New York, N. Y.) · 2020Article
- Review
- Neuroprotective efficacy of thymoquinone against amyloid beta-induced neurotoxicity in human induced pluripotent stem cell-derived cholinergic neurons.Biochemistry and biophysics reports · 2019Article
- Temporal Characterization of Neuronal Migration Behavior on Chemically Patterned Neuronal Circuits in a DefinedACS biomaterials science & engineering · 2018Article
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5 authors.
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Abstract
Alzheimer's disease (AD) is characterized by slow, progressive neurodegeneration leading to severe neurological impairment, but current drug development efforts are limited by the lack of robust, human-based disease models. Amyloid-β (Aβ) is known to play an integral role in AD progression as it has been shown to interfere with neurological function. However, studies into AD pathology commonly apply Aβ to neurons for short durations at nonphysiological concentrations to induce an exaggerated dysfunctional phenotype. Such methods are unlikely to elucidate early stage disease dysfunction, when treatment is still possible, since damage to neurons by these high concentrations is extensive. In this study, we investigated chronic, pathologically relevant Aβ oligomer concentrations to induce an electrophysiological phenotype that is more representative of early AD progression compared to an acute high-dose application in human cortical neurons. The high, acute oligomer dose resulted in severe neuronal toxicity as well as upregulation of tau and phosphorylated tau. Chronic, low-dose treatment produced significant functional impairment without increased cell death or accumulation of tau protein. This in vitro phenotype more closely mirrors the status of early stage neural decline in AD pathology and could provide a valuable tool to further understanding of early stage AD pathophysiology and for screening potential therapeutic compounds.
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