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The TMEM106B

The TMEM106B The TMEM106B locus and TDP-43 pathology in older persons without FTLD Lei Yu, PhD ABSTRACT Philip L. De Jager, MD, Objective: To determine the independent association of the TMEM106B variants with transactive PhD response DNA binding protein 43 (TDP-43) pathology in older persons without frontotemporal Jingyun Yang, PhD lobar degeneration (FTLD) and to explore functional pathways that link the risk variants to the John Q. Trojanowski, pathology, including a GRN mRNA pathway. MD, PhD Methods: Data came from 544 autopsied participants without FTLD in 2 community-based stud- David A. Bennett, MD ies of aging. Participants underwent uniform neuropathologic evaluations, including TDP-43 cyto- Julie A. Schneider, MD plasmic inclusions. We examined the association of TMEM106B variants with a semiquantitative measure of TDP-43 pathology in a series of regression analysis. We explored potential pathways by leveraging genetic, brain DNA methylation, miRNA, and transcriptomic data collected from this Correspondence to same group of participants. Dr. Schneider: [email protected] Results: TDP-43 pathology was identified in 51.7% of the participants. The index single- nucleotide polymorphism (SNP), rs1990622 , was associated with more advanced TDP-43 pathology. Top hits from fine mapping of the locus were in linkage disequilibrium of the index SNP. The association remained significant http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neurology Wolters Kluwer Health

The TMEM106B

Schneider, Julie A.
Neurology , Volume 84 (9) – Mar 1, 2015
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References (36)

Copyright
© 2015 American Academy of Neurology
ISSN
0028-3878
eISSN
1526-632X
DOI
10.1212/WNL.0000000000001313
pmid
25653292
Publisher site
See Article on Publisher Site

Abstract

The TMEM106B locus and TDP-43 pathology in older persons without FTLD Lei Yu, PhD ABSTRACT Philip L. De Jager, MD, Objective: To determine the independent association of the TMEM106B variants with transactive PhD response DNA binding protein 43 (TDP-43) pathology in older persons without frontotemporal Jingyun Yang, PhD lobar degeneration (FTLD) and to explore functional pathways that link the risk variants to the John Q. Trojanowski, pathology, including a GRN mRNA pathway. MD, PhD Methods: Data came from 544 autopsied participants without FTLD in 2 community-based stud- David A. Bennett, MD ies of aging. Participants underwent uniform neuropathologic evaluations, including TDP-43 cyto- Julie A. Schneider, MD plasmic inclusions. We examined the association of TMEM106B variants with a semiquantitative measure of TDP-43 pathology in a series of regression analysis. We explored potential pathways by leveraging genetic, brain DNA methylation, miRNA, and transcriptomic data collected from this Correspondence to same group of participants. Dr. Schneider: [email protected] Results: TDP-43 pathology was identified in 51.7% of the participants. The index single- nucleotide polymorphism (SNP), rs1990622 , was associated with more advanced TDP-43 pathology. Top hits from fine mapping of the locus were in linkage disequilibrium of the index SNP. The association remained significant

Journal

Neurology – Wolters Kluwer Health

Published: Mar 1, 2015

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