ArticleProceedings of the National Academy of Sciences of the United States of America2009
Disruption of fast axonal transport is a pathogenic mechanism for intraneuronal amyloid beta.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.
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Who cites it
123 citing papers in PubMed, 221 citations in OpenAlex.
- Amyloid-β oligomers induce differential gene expression in adult human brain slices.The Journal of biological chemistry · 2012Trial
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- CSF Proteomic Profiles Associated With White Matter Integrity in Cognitively Normal Older Adults With and Without Amyloid Pathology.Neurology · 2026Article
- Identification of 4,5,6,7-Tetrabromo-1bioRxiv : the preprint server for biology · 2026Article
- Exploring the Biological Connection Between Tau and PrPMolecular neurobiology · 2025Review
- Neuroprotective Effects of Hesperidin and CK2 Inhibitor DRB on AβMolecular neurobiology · 2025Article
- Subcellular proteomics and iPSC modeling uncover reversible mechanisms of axonal pathology in Alzheimer's disease.Nature aging · 2025Article
- Somatostatin: Linking Cognition and Alzheimer Disease to Therapeutic Targeting.Pharmacological reviews · 2024Review
- The duality of amyloid-β: its role in normal and Alzheimer's disease states.Molecular brain · 2024Review
- Unraveling the interplay of kinesin-1, tau, and microtubules in neurodegeneration associated with Alzheimer's disease.Frontiers in cellular neuroscience · 2024Review
- Using Live-Cell Imaging to Measure the Effects of Pathological Proteins on Axonal Transport in Primary Hippocampal Neurons.Journal of visualized experiments : JoVE · 2023Article
- Article
- Anti-Amyloid Immunotherapies for Alzheimer's Disease: A 2023 Clinical Update.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Amyloid β-based therapy for Alzheimer's disease: challenges, successes and future.Signal transduction and targeted therapy · 2023Review
- Glycogen synthase kinase 3β (GSK3β) and presenilin (PS) are key regulators of kinesin-1-mediated cargo motility within axons.Frontiers in cell and developmental biology · 2023Review
- Inhibition of CK2 mitigates Alzheimer's tau pathology by preventing NR2B synaptic mislocalization.Acta neuropathologica communications · 2022Article
- Casein Kinase 2 Signaling in White Matter Stroke.Frontiers in molecular biosciences · 2022Review
- Pathophysiology of neurodegenerative diseases: An interplay among axonal transport failure, oxidative stress, and inflammation?Seminars in immunology · 2022Review
- Phosphoregulation of Kinesins Involved in Long-Range Intracellular Transport.Frontiers in cell and developmental biology · 2022Review
- Graph Models of Pathology Spread in Alzheimer's Disease: An Alternative to Conventional Graph Theoretic Analysis.Brain connectivity · 2021Review
63 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The pathological mechanism by which Abeta causes neuronal dysfunction and death remains largely unknown. Deficiencies in fast axonal transport (FAT) were suggested to play a crucial role in neuronal dysfunction and loss for a diverse set of dying back neuropathologies including Alzheimer's disease (AD), but the molecular basis for pathological changes in FAT were undetermined. Recent findings indicate that soluble intracellular oligomeric Abeta (oAbeta) species may play a critical role in AD pathology. Real-time analysis of vesicle mobility in isolated axoplasms perfused with oAbeta showed bidirectional axonal transport inhibition as a consequence of endogenous casein kinase 2 (CK2) activation. Conversely, neither unaggregated amyloid beta nor fibrillar amyloid beta affected FAT. Inhibition of FAT by oAbeta was prevented by two specific pharmacological inhibitors of CK2, as well as by competition with a CK2 substrate peptide. Furthermore, perfusion of axoplasms with active CK2 mimics the inhibitory effects of oAbeta on FAT. Both oAbeta and CK2 treatment of axoplasm led to increased phosphorylation of kinesin-1 light chains and subsequent release of kinesin from its cargoes. Therefore pharmacological modulation of CK2 activity may represent a promising target for therapeutic intervention in AD.
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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.