ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2006
Abeta induces cell death by direct interaction with its cognate extracellular domain on APP (APP 597-624).
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 133 citations in OpenAlex.
- APP-C31 pathology as a target in neurodegenerative diseases.Journal of biomedical science · 2026Review
- Caspase cleavage of APP contributes to amyloid beta-protein induced synaptic injury.bioRxiv : the preprint server for biology · 2025Article
- Article
- Cholesterol and Lipid Rafts in the Biogenesis of Amyloid-β Protein and Alzheimer's Disease.Annual review of biophysics · 2024Review
- Re-Arranging the Puzzle between the Amyloid-Beta and Tau Pathology: An APP-Centric Approach.International journal of molecular sciences · 2023Review
- The brain on time: links between development and neurodegeneration.Development (Cambridge, England) · 2023Article
- Aβ Assemblies Promote Amyloidogenic Processing of APP and Intracellular Accumulation of Aβ42 Through Go/Gβγ Signaling.Frontiers in cell and developmental biology · 2022Article
- Amyloid precursor protein (APP) and amyloid β (Aβ) interact with cell adhesion molecules: Implications in Alzheimer's disease and normal physiology.Frontiers in cell and developmental biology · 2022Review
- Amyloid β and Amyloid Precursor Protein Synergistically Suppress Large-Conductance Calcium-Activated Potassium Channel in Cortical Neurons.Frontiers in aging neuroscience · 2021Article
- Tau is not necessary for amyloid-β-induced synaptic and memory impairments.The Journal of clinical investigation · 2020Article
- Accelerated Amyloid Beta Pathogenesis by Bacterial Amyloid FapC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- Effect of Aβ Oligomers on Neuronal APP Triggers a Vicious Cycle Leading to the Propagation of Synaptic Plasticity Alterations to Healthy Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Salvianolic Acid B improves cognitive impairment by inhibiting neuroinflammation and decreasing Aβ level inAging · 2020Article
- Neuromodulatory Action of Picomolar Extracellular Aβ42 Oligomers on Presynaptic and Postsynaptic Mechanisms Underlying Synaptic Function and Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Synaptic and memory dysfunction induced by tau oligomers is rescued by up-regulation of the nitric oxide cascade.Molecular neurodegeneration · 2019Article
- Structure of APP-C99Biochimica et biophysica acta. Biomembranes · 2018Article
- Prion-like propagation of β-amyloid aggregates in the absence of APP overexpression.Acta neuropathologica communications · 2018Article
- Role of Amyloid-β and Tau Proteins in Alzheimer's Disease: Confuting the Amyloid Cascade.Journal of Alzheimer's disease : JAD · 2018Review
- Human Brain-Derived Aβ Oligomers Bind to Synapses and Disrupt Synaptic Activity in a Manner That Requires APP.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Neuroprotective astrocyte-derived insulin/insulin-like growth factor 1 stimulates endocytic processing and extracellular release of neuron-bound Aβ oligomers.Molecular biology of the cell · 2017Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Amyloid beta-peptide (Abeta) is postulated to play a central role in the pathogenesis of Alzheimer's disease. We recently proposed a pathway of Abeta-induced toxicity that is APP dependent and involves the facilitation of APP complex formation by Abeta. The APP-dependent component requires cleavage of APP at position 664 in the cytoplasmic domain, presumably by caspases or caspase-like proteases, with release of a potentially cytotoxic C31 peptide. In this study we show that Abeta interacted directly and specifically with membrane-bound APP to facilitate APP homo-oligomerization. Using chimeric APP molecules, this interaction was shown to take place between Abeta and its homologous sequence on APP. Consistent with this finding, we demonstrated that Abeta also facilitated the oligomerization of beta-secretase cleaved APP C-terminal fragment (C99). We found that the YENPTY domain in the APP cytoplasmic tail and contained within C31 is critical for this cell death pathway. Deletion or alanine- scanning mutagenesis through this domain significantly attenuated cell death apparently without affecting either APP dimerization or cleavage at position 664. This indicated that sequences within C31 are required after its release from APP. As the YENPTY domain has been shown to interact with a number of cytosolic adaptor molecules, it is possible that the interaction of APP, especially dimeric forms of APP, with these molecules contribute to cell death.
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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.