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Unveiling DNA methylation in Alzheimer’s disease: a review of array-based human brain studies


Alves, Victoria Cunha; Carro, Eva; Figueiro-Silva, Joana (2024). Unveiling DNA methylation in Alzheimer’s disease: a review of array-based human brain studies. Neural Regeneration Research, 19(11):2365-2376.

Abstract

The intricacies of Alzheimer’s disease pathogenesis are being increasingly illuminated by the exploration of epigenetic mechanisms, particularly DNA methylation. This review comprehensively surveys recent human-centered studies that investigate whole genome DNA methylation in Alzheimer’s disease neuropathology. The examination of various brain regions reveals distinctive DNA methylation patterns that associate with the Braak stage and Alzheimer’s disease progression. The entorhinal cortex emerges as a focal point due to its early histological alterations and subsequent impact on downstream regions like the hippocampus. Notably, ANK1 hypermethylation, a protein implicated in neurofibrillary tangle formation, was recurrently identified in the entorhinal cortex. Further, the middle temporal gyrus and prefrontal cortex were shown to exhibit significant hypermethylation of genes like HOXA3, RHBDF2, and MCF2L, potentially influencing neuroinflammatory processes. The complex role of BIN1 in late-onset Alzheimer’s disease is underscored by its association with altered methylation patterns. Despite the disparities across studies, these findings highlight the intricate interplay between epigenetic modifications and Alzheimer’s disease pathology. Future research efforts should address methodological variations, incorporate diverse cohorts, and consider environmental factors to unravel the nuanced epigenetic landscape underlying Alzheimer’s disease progression.

Abstract

The intricacies of Alzheimer’s disease pathogenesis are being increasingly illuminated by the exploration of epigenetic mechanisms, particularly DNA methylation. This review comprehensively surveys recent human-centered studies that investigate whole genome DNA methylation in Alzheimer’s disease neuropathology. The examination of various brain regions reveals distinctive DNA methylation patterns that associate with the Braak stage and Alzheimer’s disease progression. The entorhinal cortex emerges as a focal point due to its early histological alterations and subsequent impact on downstream regions like the hippocampus. Notably, ANK1 hypermethylation, a protein implicated in neurofibrillary tangle formation, was recurrently identified in the entorhinal cortex. Further, the middle temporal gyrus and prefrontal cortex were shown to exhibit significant hypermethylation of genes like HOXA3, RHBDF2, and MCF2L, potentially influencing neuroinflammatory processes. The complex role of BIN1 in late-onset Alzheimer’s disease is underscored by its association with altered methylation patterns. Despite the disparities across studies, these findings highlight the intricate interplay between epigenetic modifications and Alzheimer’s disease pathology. Future research efforts should address methodological variations, incorporate diverse cohorts, and consider environmental factors to unravel the nuanced epigenetic landscape underlying Alzheimer’s disease progression.

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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Medical Genetics
07 Faculty of Science > Institute of Molecular Life Sciences
Dewey Decimal Classification:610 Medicine & health
570 Life sciences; biology
Uncontrolled Keywords:Developmental Neuroscience, Genetics, Genetics (clinical), Alzheimer’s disease, ANK1, BIN1, DNA methylation, epigenome-wide association studies, HOXA3, MCF2L, RHBDF2
Language:English
Date:1 November 2024
Deposited On:16 Jan 2024 11:48
Last Modified:13 Jun 2024 12:27
Publisher:Wolters Kluwer
ISSN:1673-5374
OA Status:Gold
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.4103/1673-5374.393106
Related URLs:https://api.semanticscholar.org/CorpusID:266907319 (Organisation)
Other Identification Number:Corpus ID: 266907319
  • Content: Published Version
  • Language: English
  • Licence: Creative Commons: Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)