posted on 2021-03-29, 13:15authored byAdam R Smith, Rebecca G Smith, Ruby Macdonald, Sarah J Marzi, Joe Burrage, Claire Troakes, Safa Al-Sarraj, Jonathan Mill, Katie Lunnon
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<p><b>Supplementary
Material</b>. The
histone modification H3K4me3 is altered at the ANK1 locus in Alzheimer’s
disease brain.</p>
<p> </p>
<p><u>Background</u></p>
<p>Several
epigenome-wide association studies of DNA methylation have highlighted
altered DNA methylation in the <i>ANK1 </i>gene
in Alzheimer’s disease brain samples. However, no study has specifically examined
<i>ANK1 </i>histone modifications in the
disease.</p>
<p> </p>
<p><u>Methods</u></p>
<p>We
use chromatin immunoprecipitation-qPCR to quantify tri-methylation at histone
3 lysine 4 (H3K4me3) and 27 (H3K27me3) in the <i>ANK1</i> gene in entorhinal cortex from donors with high (N= 59) or
low (N=29) Alzheimer’s pathology.</p>
<p> </p>
<p><u>Discussion</u></p>
<p>We
demonstrate decreased levels of H3K4me3, a marker of active gene
transcription, with no change in H3K27me3, a marker of inactive genes.
H3K4me3 is negatively correlated with DNA methylation in specific regions of
the <i>ANK1 </i>gene.</p>
<p> </p>
<p><u>Conclusions</u></p>
<p>Our
study suggests that the <i>ANK1 </i>gene
shows altered epigenetic marks indicative of reduced gene activation in
Alzheimer’s disease.</p>
<p> </p>
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