ReviewCell death & disease2025
Role of LIMK1-cofilin-actin axis in dendritic spine dynamics in Alzheimer's disease.
Review in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
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- Suppression of neuronal p27 impairs cognitive function in middle-aged mice.Neurobiology of disease · 2026Article
- Identifying ROCK2 as an intervention target for bilirubin encephalopathy.Fundamental research · 2026Article
- A Biomarker Out of Context: Understanding High p-tau217 in the Developing Brain.Molecular neurobiology · 2026Review
- High-fat diet leads to male reproductive dysfunction by disrupting lipid-droplet-mediated organelle crosstalk.Cellular & molecular biology letters · 2026Article
- Esketamine Alleviates Postoperative Cognitive Dysfunction via Rock2/Add1 Signaling Pathway in Aged Mice.Neurochemical research · 2026Article
- Synaptic spine head morphodynamics from graph grammar rules for actin dynamics.bioRxiv : the preprint server for biology · 2026Article
- The Electromechanical Connectome: Integrating Voltage, Mechanical Nano-Forces, and Subcellular Fluid Phase Dynamics in Human Neural Computation.International journal of molecular sciences · 2026Review
- Amyloid Beta Oligomers as Early Triggers of Neuronal Cytoskeleton Dysfunction in Alzheimer's Disease.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Systematic pan-cancer analysis reveals context-dependent prognostic and immunological roles of WDR1 with divergent effects in renal and gastric cancers.Frontiers in immunology · 2026Article
- Article
- Neuronal Actin Remodeling and Its Role in Higher Nervous Activity.International journal of molecular sciences · 2025Review
- Repurposing Cofilin-Targeting Compounds for Ischemic Stroke Through Cheminformatics and Network Pharmacology.Pharmaceuticals (Basel, Switzerland) · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Dysregulation of dendritic spine dynamics, a process essential for synaptic plasticity and memory, is a hallmark of Alzheimer's disease (AD). Actin dynamics, largely regulated by the LIMK1-cofilin pathway, are central to maintaining structural and functional stability in neurons. In healthy brains, the LIMK1-cofilin-actin axis modulates actin polymerization within dendritic spines, supporting spine growth and plasticity. However, in AD, this pathway is altered, leading to both actin and synaptic dysfunction. Studies report conflicting findings, with some indicating LIMK1 hyperactivation leading to cofilin inactivation, while others observe elevated cofilin activity, suggesting divergent regulatory mechanisms depending on the disease stage or neuronal environment. The paradoxical effects of LIMK1-cofilin signaling in AD may result from a context-dependent regulation influenced by factors such as amyloid-beta (Aβ) and tau protein accumulation, which disrupt actin dynamics and promote synaptic degeneration. The presence of cofilin-actin rods and Hirano bodies in AD highlights the role of aberrant actin stabilization and its impact on neurodegenerative processes. This review synthesizes current findings on LIMK1-cofilin-actin signaling in AD, emphasizing the dual role of cofilin in stabilizing and severing actin filaments. Targeting the LIMK1-cofilin-actin axis presents a promising therapeutic approach to restore dendritic spine dynamics and mitigate cognitive decline. However, resolving inconsistencies in cofilin regulation is essential to developing effective treatments for 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 Socratic graph.