ArticlePloS one2013
Beta-amyloid impairs reelin signaling.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 45 citations in OpenAlex.
- High reelin expression may explain why a subgroup of entorhinal cortex neurons functions as an initial nucleation site of Alzheimer's disease.PLoS computational biology · 2026Article
- Molecular links between reelin downregulation, topoisomerase IIβ alterations, and proteins involved in Alzheimer pathology in human SH-SY5Y neuroblastoma cell line.Experimental brain research · 2026Article
- Expression of Reelin, Aβ1-42, Tau and FTH1 in Idiopathic Epiretinal Membranes: Exploring the Link Between Reelin and Neurodegenerative Biomarkers.Biomolecules · 2025Article
- Intraneuronal binding of amyloid beta with reelin-Implications for the onset of Alzheimer's disease.PLoS computational biology · 2025Article
- Research progress of platelets in neurodegenerative diseases.Frontiers in aging neuroscience · 2025Review
- ApoER2-Dab1 disruption as the origin of pTau-associated neurodegeneration in sporadic Alzheimer's disease.Acta neuropathologica communications · 2023Article
- Reelin Signaling in Neurodevelopmental Disorders and Neurodegenerative Diseases.Brain sciences · 2023Review
- Review
- Lowering levels of reelin in entorhinal cortex layer II-neurons results in lowered levels of intracellular amyloid-β.Brain communications · 2023Article
- Proceedings of workshop: "Neuroglycoproteins in health and disease", INNOGLY cost action.Glycoconjugate journal · 2022Article
- Altered Balance of Reelin Proteolytic Fragments in the Cerebrospinal Fluid of Alzheimer's Disease Patients.International journal of molecular sciences · 2022Article
- Lipid Peroxidation Induced ApoE Receptor-Ligand Disruption as a Unifying Hypothesis Underlying Sporadic Alzheimer's Disease in Humans.Journal of Alzheimer's disease : JAD · 2022Article
- Morphological and biomolecular targets in retina and vitreous from Reelin-deficient mice (Reeler): Potential implications for age-related macular degeneration in Alzheimer's dementia.Frontiers in aging neuroscience · 2022Article
- Physiological significance of proteolytic processing of Reelin revealed by cleavage-resistant Reelin knock-in mice.Scientific reports · 2020Article
- Elevated Plasma Reelin Levels in Children With Autism.Frontiers in psychiatry · 2020Article
- The Reelin Receptors Apolipoprotein E receptor 2 (ApoER2) and VLDL Receptor.International journal of molecular sciences · 2018Review
- Reelin Expression in Creutzfeldt-Jakob Disease and Experimental Models of Transmissible Spongiform Encephalopathies.Molecular neurobiology · 2017Article
- Embryonic mosaic deletion of APP results in displaced Reelin-expressing cells in the cerebral cortex.Developmental biology · 2017Article
- The β-amyloid peptide compromises Reelin signaling in Alzheimer's disease.Scientific reports · 2016Article
- Therapeutic correction of ApoER2 splicing in Alzheimer's disease mice using antisense oligonucleotides.EMBO molecular medicine · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reelin is a signaling protein increasingly associated with the pathogenesis of Alzheimer's disease that relevantly modulates tau phosphorylation. We have previously demonstrated that β-amyloid peptide (Aβ) alters reelin expression. We have now attempted to determine whether abnormal reelin triggered by Aβ will result in signaling malfunction, contributing to the pathogenic process. Here, we show that reelin forms induced by β-amyloid are less capable of down-regulating tau phosphorylation via disabled-1 and GSK3β kinase. We also demonstrate that the scaffold protein 14-3-3 that increases tau phosphorylation by modulating GSK3β activity, is up-regulated during defective reelin signaling. Binding of reelin to its receptor, mainly ApoER2 in the brain, relays the signal into the cell. We associate the impaired reelin signaling with inefficiency of reelin in forming active homodimers and decreased ability to bind efficiently to its receptor, ApoER2. More remarkably, reelin from Alzheimer cortex shows a tendency to form large complexes instead of homodimers, the active form for signaling. Our results suggest that reelin expression is altered by Aβ leading to impaired reelin signaling.
Indexed as
Identifiers
What 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.