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epigenetic
274 studies tagged epigenetic, 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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46/100
While amyloid precursor protein and the microtubule-associated protein tau demonstrated higher abundance in AD brains, no significant race-related differences were observed.
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Astrocytes are crucial to brain homeostasis, yet their changes along the spatiotemporal progression of Alzheimer's disease (AD) neuropathology remain unexplored.
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16/100
The complexity of Alzheimer's disease (AD) manifests in diverse clinical phenotypes, including cognitive impairment and neuropsychiatric symptoms (NPSs).
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Parkinson's disease (PD) is a prevalent neurodegenerative disorder, and recent evidence suggests that pathogenesis may be in part mediated by inflammatory processes, the molecular and cellular architectures of which are largely unknown.
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Alzheimer's disease (AD) is a neurodegenerative disease with a projected significant increase in incidence.
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Although human cerebellum is known to be neuropathologically impaired in Alzheimer's disease (AD) and AD-related dementias (ADRD), the cell type-specific transcriptional and epigenomic changes that contribute to this pathology are not well understood.
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46/100
The emergence of single nucleus RNA sequencing (snRNA-seq) offers to revolutionize the study of Alzheimer's disease (AD).
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Chronological age offers an imperfect estimate of the molecular changes that occur with aging.
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The glucagon-like peptide-1 receptor (GLP-1R) agonists reduce glycated hemoglobin in patients with type 2 diabetes.
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Alzheimer's Disease (AD) pathology has been increasingly explored through single-cell and single-nucleus RNA-sequencing (scRNA-seq & snRNA-seq) and spatial transcriptomics (ST).
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Specifically, we first performed broad communication pattern analyses to highlight that biologically related cell types in normal brains rely on largely overlapping signaling networks and that the AD brain exhibits the irregular inter-mixing of cell types and signaling pathways.
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Alzheimer's disease (AD) is a complex neurodegenerative disorder and the most common form of dementia.
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The relationship between genetic variation and gene expression in brain cell types and subtypes remains understudied.
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Alzheimer's disease (AD) and the mechanisms underlying its etiology and progression are complex and multifactorial.
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The nervous system is one of the most complicated and enigmatic systems within the animal kingdom.
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The proliferation of single-cell RNA-sequencing data has led to the widespread use of cellular deconvolution, aiding the extraction of cell-type-specific information from extensive bulk data.
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Six miRNAs (hsa-miR-128-3p, hsa-miR-144-5p, hsa-miR-146a-5p, hsa-miR-26a-5p, hsa-miR-29c-3p and hsa-miR-363-3p) were downregulated in the blood of individuals with low cognitive performance on the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS).
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Alzheimer's disease (AD) involves degeneration of cells in the brain.
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The blood-brain barrier (BBB) is primarily manifested by a variety of physiological properties of brain endothelial cells (ECs), but the molecular foundation for these properties remains incompletely clear.
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Neuropathological lesions in the brains of individuals affected with neurodegenerative disorders are hypothesized to trigger molecular and cellular processes that disturb homeostasis of local microenvironments.
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Recent advances in single-cell transcriptomics have illuminated the diverse neuronal and glial cell types within the human brain.
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With the rapid generation of spatial transcriptomics (ST) data, integrative analysis of multiple ST datasets from different conditions, technologies and developmental stages is becoming increasingly important.
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The gene regulatory network analysis identified several hub genes regulated in AD, PD, and MS, in which HSPB1 and HSPA1A were key molecules.
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A repeat expansion in the C9orf72 (C9) gene is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
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Alzheimer's disease (AD) is the most common form of dementia worldwide, with a projection of 151 million cases by 2050.
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Cellular perturbations underlying Alzheimer's disease (AD) are primarily studied in human postmortem samples and model organisms.
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47/100
Recent work has identified dozens of non-coding loci for Alzheimer's disease (AD) risk, but their mechanisms and AD transcriptional regulatory circuitry are poorly understood.
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A diverse set of biological processes have been implicated in the pathophysiology of Alzheimer's disease (AD) and related dementias.
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The impact of alcohol abuse on Alzheimer's disease (AD) is poorly understood.
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Single cell RNA sequencing has opened a window into clarifying the complex underpinnings of disease, particularly in quantifying the relevance of tissue- and cell-type-specific gene expression.
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Biological systems are immensely complex, organized into a multi-scale hierarchy of functional units based on tightly regulated interactions between distinct molecules, cells, organs, and organisms.
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Due to commonalities in pathophysiology, age-related macular degeneration (AMD) represents a uniquely accessible model to investigate therapies for neurodegenerative diseases, leading us to examine whether pathways of disease progression are shared across neurodegenerative conditions.
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The dysfunction of astrocytes in response to environmental factors contributes to many neurological diseases by impacting neuroinflammation responses, glutamate and ion homeostasis, and cholesterol and sphingolipid metabolism, which calls for comprehensive and high-resolution analysis.
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Fusion of all five data modalities (n = 111) yielded two subtypes (n S1 = 53, n S2 = 58), which were nominally associated with diffuse amyloid plaques; however, this effect was not significant after correction for multiple testing.
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Pathogenic α-synuclein and tau are critical drivers of neurodegeneration, and their mutations cause neuronal loss in patients.
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Gaining insight into the downstream consequences of non-coding variants is an essential step towards the identification of therapeutic targets from genome-wide association study (GWAS) findings.
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Astrocytes play an important role in the pathogenesis of Alzheimer's disease (AD).
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Alzheimer's disease is the most common neurodegenerative disease, characterized by dementia and premature death.
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Complex diseases are characterized by spatiotemporal cellular and molecular changes that may be difficult to comprehensively capture.
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Cell type-specific transcriptional differences between brain tissues from donors with Alzheimer's disease (AD) and unaffected controls have been well documented, but few studies have rigorously interrogated the regulatory mechanisms responsible for these alterations.
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Synapses are crucial structures that mediate signal transmission between neurons in complex neural circuits and display considerable morphological and electrophysiological heterogeneity.
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Alzheimer's disease is the most common form of dementia.
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Spatial molecular profiling of complex tissues is essential to investigate cellular function in physiological and pathological states.
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Identifying ancestry-specific molecular profiles of late-onset Alzheimer's Disease (LOAD) in brain tissue is crucial to understand novel mechanisms and develop effective interventions in non-European, high-risk populations.
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Translating human genetic findings (genome-wide association studies [GWAS]) to pathobiology and therapeutic discovery remains a major challenge for Alzheimer's disease (AD).
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48/100
Alzheimer's disease (AD) is the most common cause of dementia with advancing age as its strongest risk factor.
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Depression is common among late-onset Alzheimer's Disease (LOAD) patients.
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The molecular diversity of glia in the human hippocampus and their temporal dynamics over the lifespan remain largely unknown.
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41/100
Firstly, we analyzed two microarray datasets related to AD (GSE48552, GSE129053) to identify the differentially expressed miRNAs, and two miRNAs were selected for further validation.
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Dysregulation of sphingomyelin and ceramide metabolism have been implicated in Alzheimer's disease.
From across this tag
6 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 6. The same 6 appear here every time.
- Identification of Vulnerable Cell Types in Major Brain Disorders Using Single Cell Transcriptomes and Expression Weighted Cell Type Enrichment
- A combined miRNA-piRNA signature to detect Alzheimer's disease
- Cell-type specific epigenetic clocks to quantify biological age at cell-type resolution
- Cell-type-directed network-correcting combination therapy for Alzheimer's disease
- Spatiotemporal transcriptomic dynamic across the auditory pathway from young to old age in 5xFAD Alzheimer disease mice
- A single-cell atlas of entorhinal cortex from individuals with Alzheimer's disease reveals cell-type-specific gene expression regulation