ReviewCurrent Alzheimer research2010
ADF/Cofilin-actin rods in neurodegenerative diseases.
Review in Current Alzheimer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.
What it found
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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
105 citing papers in PubMed, 170 citations in OpenAlex.
- Mitochondria and the Actin Cytoskeleton in Neurodegeneration.Cytoskeleton (Hoboken, N.J.) · 2026Review
- Neuronal Calcium Signaling and Cytoskeletal Dynamics in Neurodegeneration.International journal of molecular sciences · 2026Review
- Hippocampal Cofilin and CFL1 gene variants are linked to Alcohol Use Disorder phenotypes.Molecular psychiatry · 2026Article
- Transsynaptic complex dysfunction in the hippocampus of Alzheimer's disease patients.Frontiers in aging neuroscience · 2026Article
- Cytoskeletal Proteins and Alzheimer's Disease Pathogenesis: Focusing on the Interplay with Tau Pathology.Biomolecules · 2025Review
- Elevated CSF GAP-43 in Mild Cognitive Impairment Linked to Cognitive Impairment Through Increased Amyloid-β Accumulation, with a Shift to Reduced Amyloid-β Accumulation in Alzheimer's Disease.Journal of molecular neuroscience : MN · 2025Article
- Identification of actin mutants with neurodegenerative disease-like phenotypes via mutagenesis of the actin-ATP interface.Frontiers in cellular neuroscience · 2025Article
- Accumulation of F-actin drives brain aging and limits healthspan in Drosophila.Nature communications · 2024Article
- Role of Cytoskeletal Elements in Regulation of Synaptic Functions: Implications Toward Alzheimer's Disease and Phytochemicals-Based Interventions.Molecular neurobiology · 2024Review
- Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer's disease.Acta neuropathologica · 2024Article
- The Axonal Actin Filament Cytoskeleton: Structure, Function, and Relevance to Injury and Degeneration.Molecular neurobiology · 2024Review
- RABV induces biphasic actin cytoskeletal rearrangement through Rac1 activity modulation.Journal of virology · 2024Article
- Genetic admixture drives climate adaptation in the bank vole.Communications biology · 2024Article
- Actin depolymerizing factor destrin governs cell migration in neural development during Xenopus embryogenesis.Molecules and cells · 2024Article
- Bioenergetic and excitotoxic determinants of cofilactin rod formation.Journal of neurochemistry · 2024Article
- Cofilactin rod formation mediates inflammation-induced neurite degeneration.Cell reports · 2024Article
- Protein complexes from mouse and chick brain that interact with phospho-KXGS motif tau/microtubule associated protein antibody.Biology open · 2024Article
- Review
- The role of actin cytoskeleton CFL1 and ADF/cofilin superfamily in inflammatory response.Frontiers in molecular biosciences · 2024Review
- Role of Rho-associated kinases and their inhibitor fasudil in neurodegenerative diseases.Frontiers in neuroscience · 2024Review
45 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Dephosphorylation (activation) of cofilin, an actin binding protein, is stimulated by initiators of neuronal dysfunction and degeneration including oxidative stress, excitotoxic glutamate, ischemia, and soluble forms of beta-amyloid peptide (Abeta). Hyperactive cofilin forms rod-shaped cofilin-saturated actin filament bundles (rods). Other proteins are recruited to rods but are not necessary for rod formation. Neuronal cytoplasmic rods accumulate within neurites where they disrupt synaptic function and are a likely cause of synaptic loss without neuronal loss, as occurs early in dementias. Different rod-inducing stimuli target distinct neuronal populations within the hippocampus. Rods form rapidly, often in tandem arrays, in response to stress. They accumulate phosphorylated tau that immunostains for epitopes present in "striated neuropil threads," characteristic of tau pathology in Alzheimer disease (AD) brain. Thus, rods might aid in further tau modifications or assembly into paired helical filaments, the major component of neurofibrillary tangles (NFTs). Rods can occlude neurites and block vesicle transport. Some rod-inducing treatments cause an increase in secreted Abeta. Thus rods may mediate the loss of synapses, production of excess Abeta, and formation of NFTs, all of the pathological hallmarks of AD. Cofilin-actin rods also form within the nucleus of heat-shocked neurons and are cleared from cells expressing wild type huntingtin protein but not in cells expressing mutant or silenced huntingtin, suggesting a role for nuclear rods in Huntington disease (HD). As an early event in the neurodegenerative cascade, rod formation is an ideal target for therapeutic intervention that might be useful in treatment of many different neurological diseases.
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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.