ArticleCell reports2018
Extracellular Forms of Aβ and Tau from iPSC Models of Alzheimer's Disease Disrupt Synaptic Plasticity.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 85 citations in OpenAlex.
- Role of prion protein in mediating the synaptotoxic effects of tau oligomers: Implications for Alzheimer's disease and related tauopathies.Neural regeneration research · 2026Article
- Tanycytic degeneration impairs tau clearance and contributes to Alzheimer's disease pathology.Cell press blue · 2026Article
- Synaptotoxic effects of extracellular tau are mediated by its microtubule-binding region.Acta neuropathologica · 2025Article
- Current Development of iPSC-Based Modeling in Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Tau oligomers impair memory and synaptic plasticity through the cellular prion protein.Acta neuropathologica communications · 2025Article
- Rapidly reversible persistent long-term potentiation inhibition by patient-derived brain tau and amyloid ß proteins.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Article
- Synaptic protein CSF levels relate to memory scores in individuals without dementia.Research square · 2024Article
- In and out: Benchmarking in vitro, in vivo, ex vivo, and xenografting approaches for an integrative brain disease modeling pipeline.Stem cell reports · 2024Review
- Neural stem cells promote neuroplasticity: a promising therapeutic strategy for the treatment of Alzheimer's disease.Neural regeneration research · 2024Review
- Effects and mechanisms of APP and its cleavage product Aβ in the comorbidity of sarcopenia and Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Patient-derived tau and amyloid-β facilitate long-term depressionBrain communications · 2024Article
- Proteomic analysis across patient iPSC-based models and human post-mortem hippocampal tissue reveals early cellular dysfunction and progression of Alzheimer's disease pathogenesis.Acta neuropathologica communications · 2023Article
- Inducing prion protein shedding as a neuroprotective and regenerative approach in pathological conditions of the brain: from theory to facts.Neural regeneration research · 2023Review
- Tau and Amyloid β Protein in Patient-Derived Aqueous Brain Extracts Act Concomitantly to Disrupt Long-Term PotentiationThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Do tau-synaptic long-term depression interactions in the hippocampus play a pivotal role in the progression of Alzheimer's disease?Neural regeneration research · 2023Review
- Anchorless risk or released benefit? An updated view on the ADAM10-mediated shedding of the prion protein.Cell and tissue research · 2023Review
- Biogenesis, Composition and Potential Therapeutic Applications of Mesenchymal Stem Cells Derived Exosomes in Various Diseases.International journal of nanomedicine · 2023Review
- Review
- Unraveling pathological mechanisms in neurological disorders: the impact of cell-based and organoid models.Neural regeneration research · 2022Review
- Human iPSC-Derived Neural Models for Studying Alzheimer's Disease: from Neural Stem Cells to Cerebral Organoids.Stem cell reviews and reports · 2022Review
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Authors and funding
8 authors at 5 institutions in 4 countries.
Funding
Abstract
The early stages of Alzheimer's disease are associated with synaptic dysfunction prior to overt loss of neurons. To identify extracellular molecules that impair synaptic plasticity in the brain, we studied the secretomes of human iPSC-derived neuronal models of Alzheimer's disease. When introduced into the rat brain, secretomes from human neurons with either a presenilin-1 mutation, amyloid precursor protein duplication, or trisomy of chromosome 21 all strongly inhibit hippocampal long-term potentiation. Synaptic dysfunction caused by presenilin-1 mutant and amyloid precusor protein duplication secretomes is mediated by Aβ peptides, whereas trisomy of chromosome 21 (trisomy 21) neuronal secretomes induce dysfunction through extracellular tau. In all cases, synaptotoxicity is relieved by antibody blockade of cellular prion protein. These data indicate that human models of Alzheimer's disease generate distinct proteins that converge at the level of cellular prion protein to induce synaptic dysfunction in vivo.
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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.