ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Aberrant activation of focal adhesion proteins mediates fibrillar amyloid beta-induced neuronal dystrophy.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 112 citations in OpenAlex.
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- Amyloid precursor protein (APP) and amyloid β (Aβ) interact with cell adhesion molecules: Implications in Alzheimer's disease and normal physiology.Frontiers in cell and developmental biology · 2022Review
- Therapeutic Targeting of Repurposed Anticancer Drugs in Alzheimer's Disease: Using the Multiomics Approach.ACS omega · 2021Article
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- Alzheimer's, Parkinson's Disease and Amyotrophic Lateral Sclerosis Gene Expression Patterns Divergence Reveals Different Grade of RNA Metabolism Involvement.International journal of molecular sciences · 2020Article
- The new genetic landscape of Alzheimer's disease: from amyloid cascade to genetically driven synaptic failure hypothesis?Acta neuropathologica · 2019Review
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- Functional screening of Alzheimer risk loci identifies PTK2B as an in vivo modulator and early marker of Tau pathology.Molecular psychiatry · 2017Article
- Plant toxin β-ODAP activates integrin β1 and focal adhesion: A critical pathway to cause neurolathyrism.Scientific reports · 2017Article
- An Aberrant Phosphorylation of Amyloid Precursor Protein Tyrosine Regulates Its Trafficking and the Binding to the Clathrin Endocytic Complex in Neural Stem Cells of Alzheimer's Disease Patients.Frontiers in molecular neuroscience · 2017Article
- Overcoming translational barriers impeding development of Alzheimer's disease modifying therapies.Journal of neurochemistry · 2016Review
- Aβ Influences Cytoskeletal Signaling Cascades with Consequences to Alzheimer's Disease.Molecular neurobiology · 2015Review
- Ceruloplasmin functional changes in Parkinson's disease-cerebrospinal fluid.Molecular neurodegeneration · 2015Article
- Oxidation-induced structural changes of ceruloplasmin foster NGR motif deamidation that promotes integrin binding and signaling.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Neuronal dystrophy is a pathological hallmark of Alzheimer's disease (AD) that is not observed in other neurodegenerative disorders that lack amyloid deposition. Treatment of cortical neurons with fibrillar amyloid beta (Abeta) peptides induces progressive neuritic dystrophy accompanied by a marked loss of synaptophysin immunoreactivity (Grace et al., 2002). Here, we report that fibrillar Abeta-induced neuronal dystrophy is mediated by the activation of focal adhesion (FA) proteins and the formation of aberrant FA structures adjacent to Abeta deposits. In the AD brain, activated FA proteins are observed associated with the majority of senile plaques. Clustered integrin receptors and activated paxillin (phosphorylated at Tyr-31) and focal adhesion kinase (phosphorylated at Tyr-297) are mainly detected in dystrophic neurites surrounding Abeta plaque cores, where they colocalize with hyperphosphorylated tau. Deletion experiments demonstrated that the presence of the LIM domains in the paxillin C terminus and the recruitment of the protein-Tyr phosphatase (PTP)-PEST to the FA complex are required for Abeta-induced neuronal dystrophy. Therefore, both paxillin and PTP-PEST appear to be critical elements in the generation of the dystrophic response. Paxillin is a scaffolding protein to which other FA proteins bind, leading to the formation of the FA contact and initiation of signaling cascades. PTP-PEST plays a key role in the dynamic regulation of focal adhesion contacts in response to extracellular cues. Thus, in the AD brain, fibrillar Abeta may induce neuronal dystrophy by triggering a maladaptive plastic response mediated by FA protein activation and tau hyperphosphorylation.
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Identifiers
12533609PMC6741895W1562586507What 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.