Reelin protects against amyloid β toxicity in vivo
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Reelin prevents the deleterious effects of amyloid β on synaptic transmission, learning, and memory.
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Adult loss of Reelin does not cause significant cognitive impairment.
“adult loss of Reelin does not cause significant cognitive impairment”
From ApoE, ApoE Receptors, and the Synapse in Alzheimer's Disease (2017) · cites this paper as [42]
Adult loss of Reelin and ApoE receptor signaling in mice is well-tolerated in the absence of amyloid pathology, likely due to homeostatic regulation and compensation by other neuromodulatory mechanisms.
“adult loss of Reelin and ApoE receptor signaling in mice is well-tolerated in the absence of amyloid pathology, likely due to homeostatic regulation and compensation by other neuromodulatory mechanisms [42].”
From ApoE, ApoE Receptors, and the Synapse in Alzheimer's Disease (2017) · cites this paper as [42]
Overexpression of Aβ in Reelin-deficient mice leaves them heavily impaired in the Morris Water maze task of learning and memory.
“overexpression of Aβ in Reelin-deficient mice leaves them heavily impaired in the Morris Water maze task of learning and memory [42].”
From ApoE, ApoE Receptors, and the Synapse in Alzheimer's Disease (2017) · cites this paper as [42]
A role for Reelin in several neuropsychiatric and neurodegenerative diseases, such as autism, schizophrenia, bipolar disorder, major depression, and Alzheimer's disease, has been reported.
“A role for Reelin in several neuropsychiatric and neurodegenerative diseases, such as autism, schizophrenia, bipolar disorder, major depression, and Alzheimer's disease, has been reported (reviewed in Refs.20, 22, and 49).”
From Reelin: Neurodevelopmental Architect and Homeostatic Regulator of Excitatory Synapses (2017) · cites this paper as [49]
Learning deficits in an AD mouse model are exacerbated by loss of Reelin expression after development.
“Similarly, the learning deficits in an AD mouse model are exacerbated by loss of Reelin expression after development (49), further solidifying the protective role of Reelin in AD.”
From Reelin: Neurodevelopmental Architect and Homeostatic Regulator of Excitatory Synapses (2017) · cites this paper as [49]
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Self-citationThe Reelin Receptors Apolipoprotein E receptor 2 (ApoER2) and VLDL Receptor
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Hypervulnerability of the adolescent prefrontal cortex to nutritional stress via reelin deficiency
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Secreted Metalloproteinase ADAMTS-3 Inactivates Reelin
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Reelin: Diverse roles in central nervous system development, health and disease
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The β-amyloid peptide compromises Reelin signaling in Alzheimer’s disease
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NHE6 depletion corrects ApoE4-mediated synaptic impairments and reduces amyloid plaque load
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Reelin Signaling in Neurodevelopmental Disorders and Neurodegenerative Diseases
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Reelin in Alzheimer’s Disease, Increased Levels but Impaired Signaling: When More is Less
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Reelin reverts biochemical, physiological and cognitive alterations in mouse models of Tauopathy
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Reelin restricts dendritic growth of interneurons in the neocortex
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Reelin changes hippocampal learning in aging and Alzheimer’s disease
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Embryonic mosaic deletion of APP results in displaced Reelin-expressing cells in the cerebral cortex
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ADAMTS2: More than a procollagen N-proteinase
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Regulation of the hippocampal translatome by Apoer2-ICD release
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Regulatory mechanism of Reelin activity: a platform for exploiting Reelin as a therapeutic agent
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REELIN ameliorates Alzheimer's disease, but how?
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Protein retention in the endoplasmic reticulum rescues Aβ toxicity in Drosophila
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Physiologic Reelin does not play a strong role in protection against acute stroke
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Loss of endothelial CD2AP causes sex-dependent cerebrovascular dysfunction
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Reelin deficiency leads to aberrant lipid composition in mouse brain
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Two Novel Loci of RELN Associated With Antipsychotics Response in Chinese Han Population
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OCRL1 Deficiency Affects the Intracellular Traffic of ApoER2 and Impairs Reelin-Induced Responses
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Normal connectivity of thalamorecipient networks in barrel equivalents of the reeler cortex
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Safety of Anti-Reelin Therapeutic Approaches for Chronic Inflammatory Diseases
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Self-citationBiolistic transfection and expression analysis of acute cortical slices
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Self-citationGenetic variants beyond amyloid and tau associated with cognitive decline
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Reelin Regulates Developmental Desynchronization Transition of Neocortical Network Activity
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Self-citationEpilepsy-Associated Reelin Dysfunction Induces Granule Cell Dispersion in the Dentate Gyrus☆
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NHE6 depletion corrects ApoE4-mediated synaptic impairments and reduces amyloid plaque loadPreprint
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Self-citationThe Alzheimer risk factor CD2AP causes dysfunction of the brain vascular networkPreprint
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Leveraging signaling research to understand and treat disease
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Bray, N. (2015) · Nature reviews. Neuroscience · doi:10.1038/nrn4006
Science Signaling Podcast: 7 July 2015
Lane‐Donovan, C., Herz, J., & VanHook, A. M. (2015) · Science Signaling · doi:10.1126/scisignal.aac8470
Self-citationResearch progress of platelets in neurodegenerative diseases
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- Authors
- Lane-Donovan, C., Philips, G. T., Wasser, C. R., Durakoglugil, M. S., Masiulis, I., Upadhaya, A., Pohlkamp, T., Coskun, C., Kotti, T., Steller, L., Hammer, R. E., Frotscher, M., Bock, H. H., & Herz, J.
- Affiliations
- Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
- New York University (US)
- The University of Texas Southwestern Medical Center (US)
- University of Freiburg (DE)
- Institute for Structural Neurobiology, Center for Molecular Neurobiology, Hamburg 20251, Germany.
- Heinrich Heine University Düsseldorf (DE)
- Corresponding author
- Herz, Joachim
- ORCID
- Venue
- Science Signaling
- Published
- 2015-07-07
- Volume
- 8
- Issue
- 384
- Pages
- ra67-ra67
- ISSN
- 1937-9145 (ISSN-L)
- 1945-0877
- PMC
- PMC4652952
- OpenAlex
- W1904116405
- Cited by
- 96
- References
- 73
- Citations by year
- 2026: 1 · 2025: 10 · 2024: 8 · 2023: 6 · 2022: 4 · 2021: 9 · 2020: 14 · 2019: 6 · 2018: 5 · 2017: 8 · 2016: 23 · 2015: 2
- FWCI
- 9.33
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Signaling (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- FreiDok plus (Universitätsbibliothek Freiburg) (submittedVersion)
- Funders
- NIH (F30 AG047799, R37 HL63762)
- American Health Assistance Foundation
- Consortium for Frontotemporal Dementia Research
- Bright Focus Foundation
- Lupe Murchison Foundation
- The Ted Nash Long Life Foundation
- Deutsche Forschungsgemeinschaft (FR 620/12-1, SFB 780/TP5)
- Bundesministerium fur Bildung und Forschung
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- reelin, amyloid-beta, Alzheimer's disease, APOE ε4, ApoER2, VLDLR, synaptic plasticity, synaptic dysfunction, memory impairment, learning deficits, receptor recycling, neuroprotection
- MeSH terms
- Reelin Protein, Alzheimer Disease, Animals, Brain, Humans, Immunohistochemistry, Memory Disorders, Mice, Inbred C57BL, Mice, Transgenic, Motor Activity, Nerve Tissue Proteins, Receptors, LDL, Serine Endopeptidases, Blotting, Western, Cell Adhesion Molecules, Neuronal, Amyloid beta-Peptides, Extracellular Matrix Proteins, Long-Term Potentiation, Mice, Knockout, Maze Learning, LDL-Receptor Related Proteins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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