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Unmasking selective path integration deficits in Alzheimer's disease risk carriers

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Unmasking selective path integration deficits in Alzheimer's disease risk carriers. / Bierbrauer, Anne; Kunz, Lukas; Gomes, Carlos A; Luhmann, Maike; Deuker, Lorena; Getzmann, Stephan; Wascher, Edmund; Gajewski, Patrick D; Hengstler, Jan G; Fernandez-Alvarez, Marina; Atienza, Mercedes; Cammisuli, Davide M; Bonatti, Francesco; Pruneti, Carlo; Percesepe, Antonio; Bellaali, Youssef; Hanseeuw, Bernard; Strange, Bryan A; Cantero, Jose L; Axmacher, Nikolai.

in: SCI ADV, Jahrgang 6, Nr. 35, eaba1394, 08.2020.

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

Harvard

Bierbrauer, A, Kunz, L, Gomes, CA, Luhmann, M, Deuker, L, Getzmann, S, Wascher, E, Gajewski, PD, Hengstler, JG, Fernandez-Alvarez, M, Atienza, M, Cammisuli, DM, Bonatti, F, Pruneti, C, Percesepe, A, Bellaali, Y, Hanseeuw, B, Strange, BA, Cantero, JL & Axmacher, N 2020, 'Unmasking selective path integration deficits in Alzheimer's disease risk carriers', SCI ADV, Jg. 6, Nr. 35, eaba1394. https://doi.org/10.1126/sciadv.aba1394

APA

Bierbrauer, A., Kunz, L., Gomes, C. A., Luhmann, M., Deuker, L., Getzmann, S., Wascher, E., Gajewski, P. D., Hengstler, J. G., Fernandez-Alvarez, M., Atienza, M., Cammisuli, D. M., Bonatti, F., Pruneti, C., Percesepe, A., Bellaali, Y., Hanseeuw, B., Strange, B. A., Cantero, J. L., & Axmacher, N. (2020). Unmasking selective path integration deficits in Alzheimer's disease risk carriers. SCI ADV, 6(35), [eaba1394]. https://doi.org/10.1126/sciadv.aba1394

Vancouver

Bierbrauer A, Kunz L, Gomes CA, Luhmann M, Deuker L, Getzmann S et al. Unmasking selective path integration deficits in Alzheimer's disease risk carriers. SCI ADV. 2020 Aug;6(35). eaba1394. https://doi.org/10.1126/sciadv.aba1394

Bibtex

@article{09e1a5742f8e45a081930f173d35fa48,
title = "Unmasking selective path integration deficits in Alzheimer's disease risk carriers",
abstract = "Alzheimer's disease (AD) manifests with progressive memory loss and spatial disorientation. Neuropathological studies suggest early AD pathology in the entorhinal cortex (EC) of young adults at genetic risk for AD (APOE ε4-carriers). Because the EC harbors grid cells, a likely neural substrate of path integration (PI), we examined PI performance in APOE ε4-carriers during a virtual navigation task. We report a selective impairment in APOE ε4-carriers specifically when recruitment of compensatory navigational strategies via supportive spatial cues was disabled. A separate fMRI study revealed that PI performance was associated with the strength of entorhinal grid-like representations when no compensatory strategies were available, suggesting grid cell dysfunction as a mechanistic explanation for PI deficits in APOE ε4-carriers. Furthermore, posterior cingulate/retrosplenial cortex was involved in the recruitment of compensatory navigational strategies via supportive spatial cues. Our results provide evidence for selective PI deficits in AD risk carriers, decades before potential disease onset.",
keywords = "Alzheimer Disease/genetics, Apolipoprotein E4/genetics, Entorhinal Cortex, Heterozygote, Humans, Magnetic Resonance Imaging, Young Adult",
author = "Anne Bierbrauer and Lukas Kunz and Gomes, {Carlos A} and Maike Luhmann and Lorena Deuker and Stephan Getzmann and Edmund Wascher and Gajewski, {Patrick D} and Hengstler, {Jan G} and Marina Fernandez-Alvarez and Mercedes Atienza and Cammisuli, {Davide M} and Francesco Bonatti and Carlo Pruneti and Antonio Percesepe and Youssef Bellaali and Bernard Hanseeuw and Strange, {Bryan A} and Cantero, {Jose L} and Nikolai Axmacher",
note = "Copyright {\textcopyright} 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution License 4.0 (CC BY).",
year = "2020",
month = aug,
doi = "10.1126/sciadv.aba1394",
language = "English",
volume = "6",
journal = "SCI ADV",
issn = "2375-2548",
publisher = "American Association for the Advancement of Science",
number = "35",

}

RIS

TY - JOUR

T1 - Unmasking selective path integration deficits in Alzheimer's disease risk carriers

AU - Bierbrauer, Anne

AU - Kunz, Lukas

AU - Gomes, Carlos A

AU - Luhmann, Maike

AU - Deuker, Lorena

AU - Getzmann, Stephan

AU - Wascher, Edmund

AU - Gajewski, Patrick D

AU - Hengstler, Jan G

AU - Fernandez-Alvarez, Marina

AU - Atienza, Mercedes

AU - Cammisuli, Davide M

AU - Bonatti, Francesco

AU - Pruneti, Carlo

AU - Percesepe, Antonio

AU - Bellaali, Youssef

AU - Hanseeuw, Bernard

AU - Strange, Bryan A

AU - Cantero, Jose L

AU - Axmacher, Nikolai

N1 - Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution License 4.0 (CC BY).

PY - 2020/8

Y1 - 2020/8

N2 - Alzheimer's disease (AD) manifests with progressive memory loss and spatial disorientation. Neuropathological studies suggest early AD pathology in the entorhinal cortex (EC) of young adults at genetic risk for AD (APOE ε4-carriers). Because the EC harbors grid cells, a likely neural substrate of path integration (PI), we examined PI performance in APOE ε4-carriers during a virtual navigation task. We report a selective impairment in APOE ε4-carriers specifically when recruitment of compensatory navigational strategies via supportive spatial cues was disabled. A separate fMRI study revealed that PI performance was associated with the strength of entorhinal grid-like representations when no compensatory strategies were available, suggesting grid cell dysfunction as a mechanistic explanation for PI deficits in APOE ε4-carriers. Furthermore, posterior cingulate/retrosplenial cortex was involved in the recruitment of compensatory navigational strategies via supportive spatial cues. Our results provide evidence for selective PI deficits in AD risk carriers, decades before potential disease onset.

AB - Alzheimer's disease (AD) manifests with progressive memory loss and spatial disorientation. Neuropathological studies suggest early AD pathology in the entorhinal cortex (EC) of young adults at genetic risk for AD (APOE ε4-carriers). Because the EC harbors grid cells, a likely neural substrate of path integration (PI), we examined PI performance in APOE ε4-carriers during a virtual navigation task. We report a selective impairment in APOE ε4-carriers specifically when recruitment of compensatory navigational strategies via supportive spatial cues was disabled. A separate fMRI study revealed that PI performance was associated with the strength of entorhinal grid-like representations when no compensatory strategies were available, suggesting grid cell dysfunction as a mechanistic explanation for PI deficits in APOE ε4-carriers. Furthermore, posterior cingulate/retrosplenial cortex was involved in the recruitment of compensatory navigational strategies via supportive spatial cues. Our results provide evidence for selective PI deficits in AD risk carriers, decades before potential disease onset.

KW - Alzheimer Disease/genetics

KW - Apolipoprotein E4/genetics

KW - Entorhinal Cortex

KW - Heterozygote

KW - Humans

KW - Magnetic Resonance Imaging

KW - Young Adult

U2 - 10.1126/sciadv.aba1394

DO - 10.1126/sciadv.aba1394

M3 - SCORING: Journal article

C2 - 32923622

VL - 6

JO - SCI ADV

JF - SCI ADV

SN - 2375-2548

IS - 35

M1 - eaba1394

ER -