Cited by 96Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsNeuroscience and Neuropharmacology Research

Reelin protects against amyloid β toxicity in vivo

Open access
Lane-Donovan, Courtney, Philips, Gary T., Wasser, Catherine R., Durakoglugil, Murat S., Masiulis, Irene, Upadhaya, Ajeet, Pohlkamp, Theresa, Coskun, Cagil +6 more·2015·Science Signaling

Abstract

Reelin prevents the deleterious effects of amyloid β on synaptic transmission, learning, and memory.

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Integrity signals

Registry

Crossref · 10.1126/scisignal.aaa6674

Cites

72 of 72 references verified0 citation errors · 0 not checkable

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Claims other papers make about this one

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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).”
  • 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.”

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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
Venue
Science Signaling
Published
2015-07-07
Volume
8
Issue
384
Pages
ra67-ra67
ISSN
  • 1937-9145 (ISSN-L)
  • 1945-0877
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
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

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