ReviewMolecular neurobiology2015
Aβ Influences Cytoskeletal Signaling Cascades with Consequences to Alzheimer's Disease.
Review in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
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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.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- Salbutamol and Formoterol Attenuate Okadaic Acid-Induced Cytotoxicity in Undifferentiated PC-12 Cells: Evidence for a β2-Adrenergic Receptor-Independent Protective Component.Current issues in molecular biology · 2026Article
- Aβ Modulates Extracellular Vesicles Proteomic Profile Impacting Phosphorylation Mediators.Molecular neurobiology · 2025Article
- Intervertebral disc impairments in a mouse model of Alzheimer's Disease.bioRxiv : the preprint server for biology · 2025Article
- Cytoskeleton dysfunction of motor neuron in spinal muscular atrophy.Journal of neurology · 2024Review
- Review
- A proteomics analysis of 5xFAD mouse brain regions reveals the lysosome-associated protein Arl8b as a candidate biomarker for Alzheimer's disease.Genome medicine · 2023Article
- Novel therapeutic strategies targeting mitochondria as a gateway in neurodegeneration.Neural regeneration research · 2023Review
- Novel Exosome Biomarker Candidates for Alzheimer's Disease Unravelled Through Mass Spectrometry Analysis.Molecular neurobiology · 2022Article
- Synergistic influence of cytokine gene polymorphisms over the risk of dementia: A multifactor dimensionality reduction analysis.Frontiers in aging neuroscience · 2022Article
- High-Throughput Sequencing to Investigate lncRNA-circRNA-miRNA-mRNA Networks Underlying the Effects of Beta-Amyloid Peptide and Senescence on Astrocytes.Frontiers in genetics · 2022Article
- Neuromechanobiology: An Expanding Field Driven by the Force of Greater Focus.Advanced healthcare materials · 2021Review
- Role of amyloid β-peptide in the pathogenesis of age-related macular degeneration.BMJ open ophthalmology · 2021Review
- NEAT1 regulates microtubule stabilization via FZD3/GSK3β/P-tau pathway in SH-SY5Y cells and APP/PS1 mice.Aging · 2020Article
- Three-dimensional real time imaging of amyloid β aggregation on living cells.Scientific reports · 2020Article
- A Soft Mechanical Phenotype of SH-SY5Y Neuroblastoma and Primary Human Neurons Is Resilient to Oligomeric Aβ(1-42) Injury.ACS chemical neuroscience · 2020Article
- Cyclase-associated protein 2 dimerization regulates cofilin in synaptic plasticity and Alzheimer's disease.Brain communications · 2020Article
- ApoE-2 Brain-Targeted Gene Therapy Through Transferrin and Penetratin Tagged Liposomal Nanoparticles.Pharmaceutical research · 2019Article
- Cofilin, a Master Node Regulating Cytoskeletal Pathogenesis in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2019Review
- The Delivery Challenge in Neurodegenerative Disorders: The Nanoparticles Role in Alzheimer's Disease Therapeutics and Diagnostics.Pharmaceutics · 2018Review
- AD-Related N-Terminal Truncated Tau Is Sufficient to Recapitulate In Vivo the Early Perturbations of Human Neuropathology: Implications for Immunotherapy.Molecular neurobiology · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal signal transduction events can impact upon the cytoskeleton, affecting the actin and microtubule networks with direct relevance to Alzheimer's disease (AD). Cytoskeletal anomalies, in turn, promote atypical neuronal responses, with consequences for cellular organization and function. Neuronal cytoskeletal modifications in AD include neurofibrillary tangles, which result from aggregates of hyperphosphorylated tau protein. The latter is a microtubule (MT)-binding protein, whose abnormal phosphorylation leads to MT instability and consequently provokes irregularities in the neuronal trafficking pathways. Early stages of AD are also characterized by synaptic dysfunction and loss of dendritic spines, which correlate with cognitive deficit and impaired brain function. Actin dynamics has a prominent role in maintaining spine plasticity and integrity, thus providing the basis for memory and learning processes. Hence, factors that disrupt both actin and MT network dynamics will compromise neuronal function and survival. The peptide Aβ is the major component of senile plaques and has been described as a pivotal mediator of neuronal dystrophy and synaptic loss in AD. Here, we review Aβ-mediated effects on both MT and actin networks and focus on the relevance of the elicited cytoskeletal signaling events targeted in AD pathology.
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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.