ReviewCytoskeleton (Hoboken, N.J.)2016
Actin dynamics and cofilin-actin rods in alzheimer disease.
Review in Cytoskeleton (Hoboken, N.J.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 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
117 citing papers in PubMed, 170 citations in OpenAlex.
- N-Homocysteinylation of Cofilin-1 Aggravates Epileptic Pathophysiology via Disruption of Actin Dynamics.Neuroscience bulletin · 2026Article
- Form and function of actin impacts actin health and aging.iScience · 2026Article
- Evaluating pharmacological targeting of actin regulatory pathways during aging in C. elegans.Biogerontology · 2026Article
- Alterations of actin in aging.Journal of cell science · 2026Review
- Exploring peripheral immune mechanisms and potential therapeutic drugs for Alzheimer's disease.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Characterization of a cofilin mutant with high actin bundling activity in living cells.bioRxiv : the preprint server for biology · 2026Article
- Temporal- and sex-specific changes in proteasome-dependent and independent polyubiquitination in the amygdala during fear memory formation.Learning & memory (Cold Spring Harbor, N.Y.) · 2026Article
- Cofilin-1 Exacerbates Tau-Induced Mitochondrial Damage, Oxidative Stress, and Apoptosis in Alzheimer's Disease.Neurochemical research · 2026Article
- Altered tear fluid protein expression in persons with mild cognitive impairment.Journal of Alzheimer's disease : JAD · 2026Article
- Coincident Fluorescence-Burst Analysis of Actin Cargo Molecules in Secreted Single Diffusing Extracellular Vesicles From Human Induced Pluripotent Stem Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- R5 and R7 positions on fluoroquinolone scaffolds drive F-actin filament disruption.Scientific reports · 2026Article
- Synaptic and cytoskeletal CSF signatures of motor neuron disease: the role of cyclase-associated protein 2.Scientific reports · 2026Article
- Protective role of high-intensity exercise and lactate against sleep deprivation-induced alterations in hippocampal gene expression and spatial learning.Neuroscience applied · 2026Article
- Mechanistic insights into the synaptic damage-repair and regeneration processes in neurodegenerative Alzheimer's disease: phytochemicals as neuroprotective agents.Frontiers in synaptic neuroscience · 2026Review
- Editorial: Impacts of cytoskeletal dysregulation on spinogenesis.Frontiers in cellular neuroscience · 2026Article
- Elucidating molecular mechanisms governing tumor necrosis factor-alpha-mediated regulation of amyloid beta 42 uptake in blood-brain barrier endothelial cells.Molecular pharmacology · 2026Article
- Obesity-induced cofilin1 pathway dysregulation: Possible molecular links between neuroinflammation, cognitive decline, and Alzheimer's disease biomarkers.IBRO neuroscience reports · 2025Article
- Form and function of actin impacts actin health and aging.bioRxiv : the preprint server for biology · 2025Article
- Role of Tpm Isoforms Produced by theBiomolecules · 2025Article
- TIMP-1 enhances Akt and BDNF signaling in neurons to reduce synaptic and cognitive deficits in 5xFAD mouse model of Alzheimer's disease.Acta neuropathologica communications · 2025Article
57 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Cytoskeletal abnormalities and synaptic loss, typical of both familial and sporadic Alzheimer disease (AD), are induced by diverse stresses such as neuroinflammation, oxidative stress, and energetic stress, each of which may be initiated or enhanced by proinflammatory cytokines or amyloid-β (Aβ) peptides. Extracellular Aβ-containing plaques and intracellular phospho-tau-containing neurofibrillary tangles are postmortem pathologies required to confirm AD and have been the focus of most studies. However, AD brain, but not normal brain, also have increased levels of cytoplasmic rod-shaped bundles of filaments composed of ADF/cofilin-actin in a 1:1 complex (rods). Cofilin, the major ADF/cofilin isoform in mammalian neurons, severs actin filaments at low cofilin/actin ratios and stabilizes filaments at high cofilin/actin ratios. It binds cooperatively to ADP-actin subunits in F-actin. Cofilin is activated by dephosphorylation and may be oxidized in stressed neurons to form disulfide-linked dimers, required for bundling cofilin-actin filaments into stable rods. Rods form within neurites causing synaptic dysfunction by sequestering cofilin, disrupting normal actin dynamics, blocking transport, and exacerbating mitochondrial membrane potential loss. Aβ and proinflammatory cytokines induce rods through a cellular prion protein-dependent activation of NADPH oxidase and production of reactive oxygen species. Here we review recent advances in our understanding of cofilin biochemistry, rod formation, and the development of cognitive deficits. We will then discuss rod formation as a molecular pathway for synapse loss that may be common between all three prominent current AD hypotheses, thus making rods an attractive therapeutic target. © 2016 Wiley Periodicals, Inc.
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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.