ReviewMolecular neurobiology2007
Cofilin-mediated neurodegeneration in Alzheimer's disease and other amyloidopathies.
Review in Molecular neurobiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 65 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
65 citing papers in PubMed, 113 citations in OpenAlex.
- Characterization of a cofilin mutant with high actin bundling activity in living cells.bioRxiv : the preprint server for biology · 2026Article
- Mitochondria and the Actin Cytoskeleton in Neurodegeneration.Cytoskeleton (Hoboken, N.J.) · 2026Review
- The Central Role of Actin in Creutzfeldt-Jakob Disease: Unlocking Therapeutic Pathways.Molecular neurobiology · 2025Review
- HSV-1 infection induces brain cofilin hyperphosphorylation in the 5×FAD Alzheimer's Disease mouse model.bioRxiv : the preprint server for biology · 2025Article
- Resilience mechanisms underlying Alzheimer's disease.Metabolic brain disease · 2025Review
- Identification of actin mutants with neurodegenerative disease-like phenotypes via mutagenesis of the actin-ATP interface.Frontiers in cellular neuroscience · 2025Article
- Organelle abnormalities in Alzheimer's disease.Organelle (Tucson, Ariz.) · 2025Article
- Accumulation of F-actin drives brain aging and limits healthspan in Drosophila.Nature communications · 2024Article
- The Axonal Actin Filament Cytoskeleton: Structure, Function, and Relevance to Injury and Degeneration.Molecular neurobiology · 2024Review
- The role of actin cytoskeleton CFL1 and ADF/cofilin superfamily in inflammatory response.Frontiers in molecular biosciences · 2024Review
- Immunotherapy with Cleavage-Specific 12A12mAb Reduces the Tau Cleavage in Visual Cortex and Improves Visuo-Spatial Recognition Memory in Tg2576 AD Mouse Model.Pharmaceutics · 2023Article
- Cytoskeletal dysregulation and neurodegenerative disease: Formation, monitoring, and inhibition of cofilin-actin rods.Frontiers in cellular neuroscience · 2022Review
- Article
- Cofilin1 oxidation links oxidative distress to mitochondrial demise and neuronal cell death.Cell death & disease · 2021Article
- Receptor tyrosine kinase ROR1 ameliorates AβScientific reports · 2021Article
- SSH1 impedes SQSTM1/p62 flux and MAPT/Tau clearance independent of CFL (cofilin) activation.Autophagy · 2021Article
- Article
- New Insights into Cellular Functions of Nuclear Actin.Biology · 2021Review
- Formation of Cytoplasmic Actin-Cofilin Rods is Triggered by Metabolic Stress and Changes in Cellular pH.Frontiers in cell and developmental biology · 2021Article
- Rho Signaling in Synaptic Plasticity, Memory, and Brain Disorders.Frontiers in cell and developmental biology · 2021Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Transport defects may arise in various neurodegenerative diseases from failures in molecular motors, microtubule abnormalities, and the chaperone/proteasomal degradation pathway leading to aggresomal-lysosomal accumulations. These defects represent important steps in the neurodegenerative cascade, although in many cases, a clear consensus has yet to be reached regarding their causal relationship to the disease. A growing body of evidence lends support to a link between neurite transport defects in the very early stages of many neurodegenerative diseases and alterations in the organization and dynamics of the actin cytoskeleton initiated by filament dynamizing proteins in the ADF/cofilin family. This article focuses on cofilin, which in neurons under stress, including stress induced by the amyloid-beta (Abeta) 1-42 peptide, undergoes dephosphorylation (activation) and forms rod-shaped actin bundles (rods). Rods inhibit transport, are sites of amyloid precursor protein accumulation, and contribute to the pathology of Alzheimer's disease. Because rods form rapidly in response to anoxia, they could also contribute to synaptic deficits associated with ischemic brain injury (e.g., stroke). Surprisingly, cofilin undergoes phosphorylation (inactivation) in hippocampal neurons treated with Abeta1-40 at high concentrations, and these neurons undergo dystrophic morphological changes, including accumulation of pretangle phosphorylated-tau. Therefore, extremes in phosphoregulation of cofilin by different forms of Abeta may explain much of the Alzheimer's disease pathology and provide mechanisms for synaptic loss and plaque expansion.
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What OpenQuestion holds
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.