ArticleScientific reports2016
The β-amyloid peptide compromises Reelin signaling in Alzheimer's disease.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 50 citations in OpenAlex.
- Expression of Reelin, Aβ1-42, Tau and FTH1 in Idiopathic Epiretinal Membranes: Exploring the Link Between Reelin and Neurodegenerative Biomarkers.Biomolecules · 2025Article
- The Reelin receptor ApoER2 is a cargo for the adaptor protein complex AP-4: Implications for Hereditary Spastic Paraplegia.Progress in neurobiology · 2024Article
- 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
- Presenilin 1 Modulates Acetylcholinesterase Trafficking and Maturation.International journal of molecular sciences · 2023Article
- 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
- Mapping the sequence specificity of heterotypic amyloid interactions enables the identification of aggregation modifiers.Nature communications · 2022Article
- New Strategies for the Treatment of Neuropsychiatric Disorders Based on Reelin Dysfunction.International journal of molecular sciences · 2022Review
- 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
- Relevance of a Novel Circuit-Level Model of Episodic Memories to Alzheimer's Disease.International journal of molecular sciences · 2021Article
- Genetic variants beyond amyloid and tau associated with cognitive decline: A cohort study.Neurology · 2020Article
- Effects of air pollution on the nervous system and its possible role in neurodevelopmental and neurodegenerative disorders.Pharmacology & therapeutics · 2020Review
- Article
- Elevated Plasma Reelin Levels in Children With Autism.Frontiers in psychiatry · 2020Article
- Biological Hallmarks of Cancer in Alzheimer's Disease.Molecular neurobiology · 2019Review
- The Reelin Receptors Apolipoprotein E receptor 2 (ApoER2) and VLDL Receptor.International journal of molecular sciences · 2018Review
- Embryonic mosaic deletion of APP results in displaced Reelin-expressing cells in the cerebral cortex.Developmental biology · 2017Article
- Intravenous Reelin Treatment Rescues Atrophy of Spleen White Pulp and Correlates to Rescue of Forced Swim Test Immobility and Neurochemical Alterations Induced by Chronic Stress.Chronic stress (Thousand Oaks, Calif.)Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Reelin is a signaling protein that plays a crucial role in synaptic function, which expression is influenced by β-amyloid (Aβ). We show that Reelin and Aβ oligomers co-immunoprecipitated in human brain extracts and were present in the same size-exclusion chromatography fractions. Aβ treatment of cells led to increase expression of Reelin, but secreted Reelin results trapped together with Aβ aggregates. In frontal cortex extracts an increase in Reelin mRNA, and in soluble and insoluble (guanidine-extractable) Reelin protein, was associated with late Braak stages of Alzheimer's disease (AD), while expression of its receptor, ApoER2, did not change. However, Reelin-dependent induction of Dab1 phosphorylation appeared reduced in AD. In cells, Aβ reduced the capacity of Reelin to induce internalization of biotinylated ApoER2 and ApoER2 processing. Soluble proteolytic fragments of ApoER2 generated after Reelin binding can be detected in cerebrospinal fluid (CSF). Quantification of these soluble fragments in CSF could be a tool to evaluate the efficiency of Reelin signaling in the brain. These CSF-ApoER2 fragments correlated with Reelin levels only in control subjects, not in AD, where these fragments diminished. We conclude that while Reelin expression is enhanced in the Alzheimer's brain, the interaction of Reelin with Aβ hinders its biological activity.
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