PortalPublikationenReelin protects against amyloid β toxicity in vivo

Reelin protects against amyloid β toxicity in vivo

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Reelin protects against amyloid β toxicity in vivo. / Lane-Donovan, Courtney; Philips, Gary T; Wasser, Catherine R; Durakoglugil, Murat S; Masiulis, Irene; Upadhaya, Ajeet; Pohlkamp, Theresa; Coskun, Cagil; Kotti, Tiina; Steller, Laura; Hammer, Robert E; Frotscher, Michael; Bock, Hans H; Herz, Joachim.

in: SCI SIGNAL, Jahrgang 8, Nr. 384, 07.07.2015, S. ra67.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Lane-Donovan, C, Philips, GT, Wasser, CR, Durakoglugil, MS, Masiulis, I, Upadhaya, A, Pohlkamp, T, Coskun, C, Kotti, T, Steller, L, Hammer, RE, Frotscher, M, Bock, HH & Herz, J 2015, 'Reelin protects against amyloid β toxicity in vivo', SCI SIGNAL, Jg. 8, Nr. 384, S. ra67. https://doi.org/10.1126/scisignal.aaa6674

APA

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. (2015). Reelin protects against amyloid β toxicity in vivo. SCI SIGNAL, 8(384), ra67. https://doi.org/10.1126/scisignal.aaa6674

Vancouver

Lane-Donovan C, Philips GT, Wasser CR, Durakoglugil MS, Masiulis I, Upadhaya A et al. Reelin protects against amyloid β toxicity in vivo. SCI SIGNAL. 2015 Jul 7;8(384):ra67. https://doi.org/10.1126/scisignal.aaa6674

Bibtex

@article{19868474b2a74de287be4a7cbf02681b,
title = "Reelin protects against amyloid β toxicity in vivo",
abstract = "Alzheimer's disease (AD) is a currently incurable neurodegenerative disorder and is the most common form of dementia in people over the age of 65 years. The predominant genetic risk factor for AD is the ε4 allele encoding apolipoprotein E (ApoE4). The secreted glycoprotein Reelin enhances synaptic plasticity by binding to the multifunctional ApoE receptors apolipoprotein E receptor 2 (Apoer2) and very low density lipoprotein receptor (Vldlr). We have previously shown that the presence of ApoE4 renders neurons unresponsive to Reelin by impairing the recycling of the receptors, thereby decreasing its protective effects against amyloid β (Aβ) oligomer-induced synaptic toxicity in vitro. We showed that when Reelin was knocked out in adult mice, these mice behaved normally without overt learning or memory deficits. However, they were strikingly sensitive to amyloid-induced synaptic suppression and had profound memory and learning disabilities with very low amounts of amyloid deposition. Our findings highlight the physiological importance of Reelin in protecting the brain against Aβ-induced synaptic dysfunction and memory impairment.",
author = "Courtney Lane-Donovan and Philips, {Gary T} and Wasser, {Catherine R} and Durakoglugil, {Murat S} and Irene Masiulis and Ajeet Upadhaya and Theresa Pohlkamp and Cagil Coskun and Tiina Kotti and Laura Steller and Hammer, {Robert E} and Michael Frotscher and Bock, {Hans H} and Joachim Herz",
note = "Copyright {\textcopyright} 2015, American Association for the Advancement of Science.",
year = "2015",
month = jul,
day = "7",
doi = "10.1126/scisignal.aaa6674",
language = "English",
volume = "8",
pages = "ra67",
journal = "SCI SIGNAL",
issn = "1945-0877",
publisher = "American Association for the Advancement of Science",
number = "384",

}

RIS

TY - JOUR

T1 - Reelin protects against amyloid β toxicity in vivo

AU - Lane-Donovan, Courtney

AU - Philips, Gary T

AU - Wasser, Catherine R

AU - Durakoglugil, Murat S

AU - Masiulis, Irene

AU - Upadhaya, Ajeet

AU - Pohlkamp, Theresa

AU - Coskun, Cagil

AU - Kotti, Tiina

AU - Steller, Laura

AU - Hammer, Robert E

AU - Frotscher, Michael

AU - Bock, Hans H

AU - Herz, Joachim

N1 - Copyright © 2015, American Association for the Advancement of Science.

PY - 2015/7/7

Y1 - 2015/7/7

N2 - Alzheimer's disease (AD) is a currently incurable neurodegenerative disorder and is the most common form of dementia in people over the age of 65 years. The predominant genetic risk factor for AD is the ε4 allele encoding apolipoprotein E (ApoE4). The secreted glycoprotein Reelin enhances synaptic plasticity by binding to the multifunctional ApoE receptors apolipoprotein E receptor 2 (Apoer2) and very low density lipoprotein receptor (Vldlr). We have previously shown that the presence of ApoE4 renders neurons unresponsive to Reelin by impairing the recycling of the receptors, thereby decreasing its protective effects against amyloid β (Aβ) oligomer-induced synaptic toxicity in vitro. We showed that when Reelin was knocked out in adult mice, these mice behaved normally without overt learning or memory deficits. However, they were strikingly sensitive to amyloid-induced synaptic suppression and had profound memory and learning disabilities with very low amounts of amyloid deposition. Our findings highlight the physiological importance of Reelin in protecting the brain against Aβ-induced synaptic dysfunction and memory impairment.

AB - Alzheimer's disease (AD) is a currently incurable neurodegenerative disorder and is the most common form of dementia in people over the age of 65 years. The predominant genetic risk factor for AD is the ε4 allele encoding apolipoprotein E (ApoE4). The secreted glycoprotein Reelin enhances synaptic plasticity by binding to the multifunctional ApoE receptors apolipoprotein E receptor 2 (Apoer2) and very low density lipoprotein receptor (Vldlr). We have previously shown that the presence of ApoE4 renders neurons unresponsive to Reelin by impairing the recycling of the receptors, thereby decreasing its protective effects against amyloid β (Aβ) oligomer-induced synaptic toxicity in vitro. We showed that when Reelin was knocked out in adult mice, these mice behaved normally without overt learning or memory deficits. However, they were strikingly sensitive to amyloid-induced synaptic suppression and had profound memory and learning disabilities with very low amounts of amyloid deposition. Our findings highlight the physiological importance of Reelin in protecting the brain against Aβ-induced synaptic dysfunction and memory impairment.

U2 - 10.1126/scisignal.aaa6674

DO - 10.1126/scisignal.aaa6674

M3 - SCORING: Journal article

C2 - 26152694

VL - 8

SP - ra67

JO - SCI SIGNAL

JF - SCI SIGNAL

SN - 1945-0877

IS - 384

ER -