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methylation
274 studies tagged methylation, dated 1997-10-01 to 2026-10-30. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- Integrative systems biology identifies shared neuroimmune co-expression programmes across pulmonary tuberculosis and Alzheimer's disease 2026-10-30
- Pregnancy History and Loss of Normal PSEN2 Function Impact Female Late-Life Cognitive Processing, Inhibitory Signaling, and Gliosis 2026-10-30
- Joint localization and testing reveals spatial context of differential expression 2026-10-29
Studies
274 studies carry this tag.
Date range
1997 to 2026
Top journals
- bioRxiv 44
- Research Square 16
- Nature neuroscience 11
- Nature communications 10
- Neuron 10
98 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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An overview of miRNAs altered in Alzheimer's disease (AD) was established by profiling the hippocampus of a cohort of 41 late-onset AD (LOAD) patients and 23 controls, showing deregulation of 35 miRNAs.
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The UPR is activated in disease affected regions in PSP and the genetic evidence shows that this activation increases risk for PSP and is not a protective response.
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The pathophysiological changes associated with Alzheimer's Disease (AD) begin decades before the emergence of clinical symptoms.
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Epigenetic dysregulation of gene expression is thought to be critically involved in the pathophysiology of Alzheimer's disease (AD).
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Overall, our analysis revealed a robustly defined age-related co-methylation module that is present in multiple human tissues, including blood and brain.
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DNA methylation is a major control program that modulates gene expression in a plethora of organisms.
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40/100
Alzheimer's disease (AD) and bipolar disorder (BD) are progressive brain disorders.
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Cognitive decline is a debilitating feature of most neurodegenerative diseases of the central nervous system, including Alzheimer's disease.
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Hereditary diffuse leukoencephalopathy with spheroids (HDLS) is an autosomal-dominant central nervous system white-matter disease with variable clinical presentations, including personality and behavioral changes, dementia, depression, parkinsonism, seizures and other phenotypes.
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Neurodegeneration in the brains of Huntington's disease patients is accompanied by widespread changes in gene regulatory networks.
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DNA methyltransferase 1 (DNMT1) is crucial for maintenance of methylation, gene regulation and chromatin stability.
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Recent studies strongly indicate that aberrations in the control of gene expression might contribute to the initiation and progression of Alzheimer's disease (AD).
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Epigenetic mechanisms such as DNA methylation and modifications to histone proteins regulate high-order DNA structure and gene expression.
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DNA methylation is a vital component of the epigenetic machinery that orchestrates changes in multiple genes and helps regulate gene expression in all known vertebrates.
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Despite an enormous research effort, most cases of late-onset Alzheimer's disease (LOAD) still remain unexplained and the current biomedical science is still a long way from the ultimate goal of revealing clear risk factors that can help in the diagnosis, prevention and treatment of the disease.
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MicroRNAs have essential functional roles in brain development and neuronal specification but their roles in neurodegenerative diseases such as Alzheimer's disease (AD) is unknown.
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The role of DNA cytosine methylation, an epigenetic regulator of chromatin structure and function, during normal and pathological brain development and aging remains unclear.
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Accurate and rapid identification of perturbed pathways through the analysis of genome-wide expression profiles facilitates the generation of biological hypotheses.
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The ageing of the human brain is a cause of cognitive decline in the elderly and the major risk factor for Alzheimer's disease.
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The pathogenesis of incipient Alzheimer's disease (AD) has been resistant to analysis because of the complexity of AD and the overlap of its early-stage markers with normal aging.
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Over the course of an individual’s lifetime, genomic alterations accumulate in somatic cells.
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Alterations in transcription, RNA editing, translation, protein processing, and clearance are a consistent feature of Alzheimer's disease (AD) brain.
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The need for methods to identify disease biomarkers is underscored by the survival-rate of patients diagnosed at early stages of cancer progression.
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Mutant presenilins have been found to cause Alzheimer disease.
From across this tag
8 of the 274 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 8. The same 8 appear here every time.
- Single-cell epigenomic analyses implicate candidate causal variants at inherited risk loci for Alzheimer's and Parkinson's diseases
- A single-cell atlas of entorhinal cortex from individuals with Alzheimer's disease reveals cell-type-specific gene expression regulation
- Deep Multilayer Brain Proteomics Identifies Molecular Networks in Alzheimer's Disease Progression
- The effects of Arf4 gene knockdown on Alzheimer's amyloid β deposition: Possible role in cognitive resilience
- Spatial Transcriptomics and In Situ Sequencing to Study Alzheimer's Disease
- Proteomic landscape of Alzheimer's Disease: novel insights into pathogenesis and biomarker discovery
- A novel multi-tissue RNA diagnostic of healthy ageing relates to cognitive health status
- Expanding RNAi therapeutics to extrahepatic tissues with lipophilic conjugates