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Original Contribution | July 2012

Effect of Genetic Variation in LRRTM3 on Risk of Alzheimer Disease

Christiane Reitz, MD, PhD; Christopher Conrad, PhD; Katherine Roszkowski; Robert S. Rogers; Richard Mayeux, MD, MSc

Arch Neurol. 2012;69(7):894-900. doi:10.1001/archneurol.2011.2463.

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ABSTRACT

Reitz and colleagues explore the role of leucine-rich repeat transmembrane 3 in late-onset Alzheimer disease by independent genetic epidemiologic and functional studies.

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Figure 1. Linkage disequilibrium (LD) patterns of single-nucleotide polymorphisms (SNPs) rs16923760, rs1925608, rs7082306, and rs1925609 in LLRTM3. A, National Institute on Aging Late-Onset Alzheimer's Disease data set (control subjects); B, Caribbean Hispanic data set (controls). Bold font indicates SNPs that are in high LD.

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Figure 2. γ-Secretase activity and nuclear translocation of amyloid precursor protein (APP) assays with leucine-rich repeat transmembrane 3 (LRRTM3) small-hairpin RNAs (shRNAs). The luciferase-based assay³⁰ consisting of the APP gene's C-terminus (AICD) fused to a transcription factor composed of the GAL4 DNA binding domain with VP16 transcriptional activator (GV) and called the APP-GV assay was performed in the HEK293 cell lines. The data from 5 shRNA LRRTM3 (TM3-shRNA) were normalized to APP-GV with the scrambled sequence shRNA that was included as a negative control. The data are representative for the APP-GV assays, and the assay has been performed in at least 3 separate experiments in replicates of 8 samples per condition (96-well format). Error bars represent SDs. * P < .01 compared with scrambled shRNA/APP-GV only (analysis of variance [GraphPad software]). † P < .05.

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Reitz C, Conrad C, Roszkowski K, Rogers RS, Mayeux R. Effect of Genetic Variation in LRRTM3 on Risk of Alzheimer Disease. Arch Neurol. 2012;69(7):894-900. doi:10.1001/archneurol.2011.2463.

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