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  • ADJ-D-16-00588R2-2

    Rights statement: This is the author’s version of a work that was accepted for publication in Alzheimer's & Dementia. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Alzheimer's & Dementia, 13, (10), 2017 DOI: 10.1016/j.jalz.2017.01.027

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Genetic epistasis regulates amyloid deposition in resilient aging

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Genetic epistasis regulates amyloid deposition in resilient aging. / Felsky, Daniel; Xu, Jishu; Chibnik, Lori et al.
In: Alzheimer's and Dementia, Vol. 13, No. 10, 10.2017, p. 1107-1116.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

Felsky, D, Xu, J, Chibnik, L, Schneider, J, Knight, J, Kennedy, JL, Bennett, DA, De Jager, PL & Voineskos, AN 2017, 'Genetic epistasis regulates amyloid deposition in resilient aging', Alzheimer's and Dementia, vol. 13, no. 10, pp. 1107-1116. https://doi.org/10.1016/j.jalz.2017.01.027

APA

Felsky, D., Xu, J., Chibnik, L., Schneider, J., Knight, J., Kennedy, J. L., Bennett, D. A., De Jager, P. L., & Voineskos, A. N. (2017). Genetic epistasis regulates amyloid deposition in resilient aging. Alzheimer's and Dementia, 13(10), 1107-1116. https://doi.org/10.1016/j.jalz.2017.01.027

Vancouver

Felsky D, Xu J, Chibnik L, Schneider J, Knight J, Kennedy JL et al. Genetic epistasis regulates amyloid deposition in resilient aging. Alzheimer's and Dementia. 2017 Oct;13(10):1107-1116. Epub 2017 Mar 17. doi: 10.1016/j.jalz.2017.01.027

Author

Felsky, Daniel ; Xu, Jishu ; Chibnik, Lori et al. / Genetic epistasis regulates amyloid deposition in resilient aging. In: Alzheimer's and Dementia. 2017 ; Vol. 13, No. 10. pp. 1107-1116.

Bibtex

@article{eb34e8caebf341eca8c89111ca2e3913,
title = "Genetic epistasis regulates amyloid deposition in resilient aging",
abstract = "AbstractIntroduction The brain-derived neurotrophic factor (BDNF) interacts with important genetic Alzheimer's disease (AD) risk factors. Specifically, variants within the SORL1 gene determine BDNF's ability to reduce amyloid β (Aβ) in vitro. We sought to test whether functional BDNF variation interacts with SORL1 genotypes to influence expression and downstream AD-related processes in humans. Methods We analyzed postmortem brain RNA sequencing and neuropathological data for 441 subjects from the Religious Orders Study/Memory and Aging Project and molecular and structural neuroimaging data for 1285 subjects from the Alzheimer's Disease Neuroimaging Initiative. Results We found one SORL1 RNA transcript strongly regulated by SORL1-BDNF interactions in elderly without pathological AD and showing stronger associations with diffuse than neuritic Aβ plaques. The same SORL1-BDNF interactions also significantly influenced Aβ load as measured with [18F]Florbetapir positron emission tomography. Discussion Our results bridge the gap between risk and resilience factors for AD, demonstrating interdependent roles of established SORL1 and BDNF functional genotypes.",
keywords = "Alzheimer's disease, Epistasis, RNA sequencing, Amyloid, BDNF, SORL1, PET imaging",
author = "Daniel Felsky and Jishu Xu and Lori Chibnik and Julie Schneider and Jo Knight and Kennedy, {James L.} and Bennett, {David A.} and {De Jager}, {Philip L.} and Voineskos, {Aristotle N.}",
note = "This is the author{\textquoteright}s version of a work that was accepted for publication in Alzheimer's & Dementia. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Alzheimer's & Dementia, 13, (10), 2017 DOI: 10.1016/j.jalz.2017.01.027",
year = "2017",
month = oct,
doi = "10.1016/j.jalz.2017.01.027",
language = "English",
volume = "13",
pages = "1107--1116",
journal = "Alzheimer's and Dementia",
issn = "1552-5260",
publisher = "Wiley",
number = "10",

}

RIS

TY - JOUR

T1 - Genetic epistasis regulates amyloid deposition in resilient aging

AU - Felsky, Daniel

AU - Xu, Jishu

AU - Chibnik, Lori

AU - Schneider, Julie

AU - Knight, Jo

AU - Kennedy, James L.

AU - Bennett, David A.

AU - De Jager, Philip L.

AU - Voineskos, Aristotle N.

N1 - This is the author’s version of a work that was accepted for publication in Alzheimer's & Dementia. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Alzheimer's & Dementia, 13, (10), 2017 DOI: 10.1016/j.jalz.2017.01.027

PY - 2017/10

Y1 - 2017/10

N2 - AbstractIntroduction The brain-derived neurotrophic factor (BDNF) interacts with important genetic Alzheimer's disease (AD) risk factors. Specifically, variants within the SORL1 gene determine BDNF's ability to reduce amyloid β (Aβ) in vitro. We sought to test whether functional BDNF variation interacts with SORL1 genotypes to influence expression and downstream AD-related processes in humans. Methods We analyzed postmortem brain RNA sequencing and neuropathological data for 441 subjects from the Religious Orders Study/Memory and Aging Project and molecular and structural neuroimaging data for 1285 subjects from the Alzheimer's Disease Neuroimaging Initiative. Results We found one SORL1 RNA transcript strongly regulated by SORL1-BDNF interactions in elderly without pathological AD and showing stronger associations with diffuse than neuritic Aβ plaques. The same SORL1-BDNF interactions also significantly influenced Aβ load as measured with [18F]Florbetapir positron emission tomography. Discussion Our results bridge the gap between risk and resilience factors for AD, demonstrating interdependent roles of established SORL1 and BDNF functional genotypes.

AB - AbstractIntroduction The brain-derived neurotrophic factor (BDNF) interacts with important genetic Alzheimer's disease (AD) risk factors. Specifically, variants within the SORL1 gene determine BDNF's ability to reduce amyloid β (Aβ) in vitro. We sought to test whether functional BDNF variation interacts with SORL1 genotypes to influence expression and downstream AD-related processes in humans. Methods We analyzed postmortem brain RNA sequencing and neuropathological data for 441 subjects from the Religious Orders Study/Memory and Aging Project and molecular and structural neuroimaging data for 1285 subjects from the Alzheimer's Disease Neuroimaging Initiative. Results We found one SORL1 RNA transcript strongly regulated by SORL1-BDNF interactions in elderly without pathological AD and showing stronger associations with diffuse than neuritic Aβ plaques. The same SORL1-BDNF interactions also significantly influenced Aβ load as measured with [18F]Florbetapir positron emission tomography. Discussion Our results bridge the gap between risk and resilience factors for AD, demonstrating interdependent roles of established SORL1 and BDNF functional genotypes.

KW - Alzheimer's disease

KW - Epistasis

KW - RNA sequencing

KW - Amyloid

KW - BDNF

KW - SORL1

KW - PET imaging

U2 - 10.1016/j.jalz.2017.01.027

DO - 10.1016/j.jalz.2017.01.027

M3 - Journal article

VL - 13

SP - 1107

EP - 1116

JO - Alzheimer's and Dementia

JF - Alzheimer's and Dementia

SN - 1552-5260

IS - 10

ER -