ArticleFrontiers in molecular neuroscience2017
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.
Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 20 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
20 citing papers in PubMed, 33 citations in OpenAlex.
- Cholesterol and Lipid Rafts in the Biogenesis of Amyloid-β Protein and Alzheimer's Disease.Annual review of biophysics · 2024Review
- Lysosomal dysfunction in Down syndrome and Alzheimer mouse models is caused by v-ATPase inhibition by TyrScience advances · 2023Article
- Beta-Secretase 1 Recruits Amyloid-Beta Precursor Protein to ROCK2 Kinase, Resulting in Erroneous Phosphorylation and Beta-Amyloid Plaque Formation.International journal of molecular sciences · 2023Article
- Pathway-specific polygenic risk scores correlate with clinical status and Alzheimer's-related biomarkers.Research square · 2023Article
- Pathway-Specific Polygenic Risk Scores Correlate with Clinical Status and Alzheimer's Disease-Related Biomarkers.Journal of Alzheimer's disease : JAD · 2023Article
- An increase in Semaphorin 3A biases the axonal direction and induces an aberrant dendritic arborization in an in vitro model of human neural progenitor differentiation.Cell & bioscience · 2022Article
- Fyn Kinase Activity and Its Role in Neurodegenerative Disease Pathology: a Potential Universal Target?Molecular neurobiology · 2021Review
- Article
- Challenges in LC-MS-based metabolomics for Alzheimer's disease early detection: targeted approaches versus untargeted approaches.Metabolomics : Official journal of the Metabolomic Society · 2021Review
- Review
- Might Fibroblasts from Patients with Alzheimer's Disease Reflect the Brain Pathology? A Focus on the Increased Phosphorylation of Amyloid Precursor Protein TyrBrain sciences · 2021Article
- Phosphoproteomics identifies microglial Siglec-F inflammatory response during neurodegeneration.Molecular systems biology · 2020Article
- Article
- Fyn Tyrosine Kinase as Harmonizing Factor in Neuronal Functions and Dysfunctions.International journal of molecular sciences · 2020Review
- The MUC6/AP2A2 Locus and Its Relevance to Alzheimer's Disease: A Review.Journal of neuropathology and experimental neurology · 2020Review
- Targeting dementias through cancer kinases inhibition.Alzheimer's & dementia (New York, N. Y.) · 2020Article
- Phosphorylation Signaling in APP Processing in Alzheimer's Disease.International journal of molecular sciences · 2019Review
- Structure of APP-C99Biochimica et biophysica acta. Biomembranes · 2018Article
- Axonal Degeneration during Aging and Its Functional Role in Neurodegenerative Disorders.Frontiers in neuroscience · 2017Review
- Disturbances in PP2A methylation and one-carbon metabolism compromise Fyn distribution, neuritogenesis, and APP regulation.The Journal of biological chemistryArticle
Corrections and comments
- Retraction · 2023-09-07Concerns/Issues about Image · Duplication of/in Image · Investigation by Journal/Publisher · Manipulation of Images · Unreliable Data · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common cause of dementia and is likely caused by defective amyloid precursor protein (APP) trafficking and processing in neurons leading to amyloid plaques containing the amyloid-β (Aβ) APP peptide byproducts. Understanding how APP is targeted to selected destinations inside neurons and identifying the mechanisms responsible for the generation of Aβ are thus the keys for the advancement of new therapies. We previously developed a mouse model with a mutation at tyrosine (Tyr) 682 in the C-terminus of APP. This residue is needed for APP to bind to the coating protein Clathrin and to the Clathrin adaptor protein AP2 as well as for the correct APP trafficking and sorting in neurons. By extending these findings to humans, we found that APP binding to Clathrin is decreased in neural stem cells from AD sufferers. Increased APP Tyr phosphorylation alters APP trafficking in AD neurons and it is associated to Fyn Tyr kinase activation. We show that compounds affecting Tyr kinase activity and counteracting defects in AD neurons can control APP location and compartmentalization. APP Tyr phosphorylation is thus a potential therapeutic target 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 OpenQuestion graph.