Locus-Associated Mitochondrial Function and Its Implication in Alzheimer's Disease and Aging.

The Apolipoprotein E ( locus has garnered significant clinical interest because of its association with Alzheimer's disease (AD) and longevity. This genetic association appears across multiple genes in the locus. Despite the apparent differences between AD and longevity, both conditions share a commonality of aging-related changes in mitochondrial function.

A Preliminary Comparison of the Methylome and Transcriptome from the Prefrontal Cortex Across Alzheimer's Disease and Lewy Body Dementia.

Background: Pathological amyloid-β and -synuclein are associated with a spectrum of related dementias, ranging from Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) to Parkinson disease dementia (PDD). While these diseases share clinical and pathological features, they also have unique patterns of pathology. However, epigenetic factors that contribute to these pathological differences remain unknown.

RNA Transcription in Alzheimer's Disease Brain and Its Implication in Mitochondrial Dysfunction.

Increasing evidence suggests that the Translocase of Outer Mitochondria Membrane 40 () gene may contribute to the risk of Alzheimer's disease (AD). Currently, there is no consensus as to whether expression is up- or down-regulated in AD brains, hindering a clear interpretation of 's role in this disease. The aim of this study was to determine if RNA levels differ between AD and control brains.

Redefining transcriptional regulation of the APOE gene and its association with Alzheimer's disease.

The apolipoprotein E gene (APOE) is the strongest genetic risk factor for late-onset Alzheimer's disease (AD), yet the expression of APOE is not clearly understood. For example, it is unclear whether AD patients have elevated or decreased APOE expression or why the correlation levels of APOE RNA and the ApoE protein differ across studies. Likewise, APOE has a single CpG island (CGI) that overlaps with its 3'-exon, and this CGI's effect is unknown.

Glia-specific APOE epigenetic changes in the Alzheimer's disease brain.

The apolipoprotein E gene (APOE) is the strongest genetic risk factor for developing Alzheimer's disease (AD). Our recent identification of altered APOE DNA methylation in AD postmortem brain (PMB) prompted this follow-up study. Our goals were to (i) validate the AD-differential methylation of APOE in an independent PMB study cohort and (ii) determine the cellular populations (i.

APOE DNA methylation is altered in Lewy body dementia.

Introduction: 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.