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APOE DNA methylation is altered in Lewy body dementia
Author(s) -
Tulloch Jessica,
Leong Lesley,
Chen Sunny,
Keene C. Dirk,
Millard Steven P.,
ShutesDavid Andrew,
Lopez Oscar L.,
Kofler Julia,
Kaye Jeffrey A.,
Woltjer Randy,
Nelson Peter T.,
Neltner Janna H.,
Jicha Gregory A.,
Galasko Douglas,
Masliah Eliezer,
Leverenz James B.,
Yu ChangEn,
Tsuang Debby
Publication year - 2018
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2018.02.005
Subject(s) - apolipoprotein e , dna methylation , epigenetics , lewy body , methylation , dementia , biology , alzheimer's disease , dementia with lewy bodies , genetics , medicine , disease , dna , gene , gene expression
Inheritance of the ε4 allele of apolipoprotein E ( APOE ) increases a person's risk of developing both Alzheimer's disease (AD) and Lewy body dementia (LBD), yet the underlying mechanisms behind this risk are incompletely understood. The recent identification of reduced APOE DNA methylation in AD postmortem brains prompted this study to investigate APOE methylation in LBD. Methods Genomic DNA from postmortem brain tissues (frontal lobe and cerebellum) of neuropathological pure (np) controls and npAD, LBD + AD, and npLBD subjects were bisulfite pyrosequenced. DNA methylation levels of two APOE subregions were then compared for these groups. Results APOE DNA methylation was significantly reduced in npLBD compared with np controls, and methylation levels were lowest in the LBD + AD group. Discussion Given that npLBD and npAD postmortem brains shared a similar reduction in APOE methylation, it is possible that an aberrant epigenetic change in APOE is linked to risk for both diseases.