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transcriptomic
274 studies tagged transcriptomic, 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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Active PTB was associated with widespread transcriptional remodeling, with 1,389 dysregulated genes organized into 16 PTB-associated co-expression modules.
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This work suggests that although parity history and PSEN2 deficiency exert individual differing age-related effects on cognition and neurobiology, they do not act synergistically.
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Multi-subject spatial transcriptomics is increasingly used to identify molecular differences across individuals and conditions while resolving where in tissue those differences occur.
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Although Alzheimer’s disease (AD) and glioblastoma (GBM) share common aging-related risk factors, they lead to opposite cellular fates—neurodegeneration versus uncontrolled proliferation.
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Current Alzheimer’s disease (AD) neuropathological metrics, including Thal phasing, and Braak staging, often do not accurately predict cognitive status: many cognitively resilient individuals have substantial pathological burdens, whereas some patients with dementia show minimal classical AD pathology.
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16/100
Single-nucleus RNA-seq (snRNA-seq) studies of Alzheimer’s disease (AD) routinely filter nuclei by mitochondrial percentage (%MT) or remove mitochondrial genes, yet whether these reads carry information about cognition is rarely examined.
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Computational drug repurposing commonly relies on transcriptomic signature matching to identify compounds that reverse disease-associated gene expression, but such approaches do not distinguish putative causal drivers from downstream consequences of disease.
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Alzheimer’s disease (AD) develops over decades, but biological processes underlying susceptibility during midlife remain poorly understood.
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DNA cytosine modifications play a crucial role in gene regulation that underlies the pathogenesis of complex diseases such as Alzheimer’s disease (AD).
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For a long time, the protein coding potential of our genome was underestimated.
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Alzheimer’s disease (AD) is a progressive, neurodegenerative disorder and the leading cause of dementia worldwide.
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In spatial proteomics across large cohorts, downstream estimates from tens of thousands of images depend on accurate cell segmentation.
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While single-cell measurements of the Alzheimer’s disease (AD) brain allow investigation of vulnerable cells in unprecedented depth, reported findings are heterogeneous, mostly descriptive and often ignore interdependence of cellular responses.
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Transcriptomic and proteomic studies have consistently demonstrated substantial molecular heterogeneity across patients with Alzheimer’s disease (AD) and other neurodegenerative disorders, leading to the proposal of multiple disease subtypes.
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Alzheimer’s disease (AD) staging based on amyloid-β, tau, and neurodegeneration does not capture heterogeneous microglial functions.
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Alzheimer’s disease (AD) is a progressive neurodegenerative disorder, in which epitranscriptomic modifications, especially RNA methylation, may exert crucial regulatory effects.
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How amyloid-β (Aβ) plaques and tau phosphorylation spatially relate to cell response and genetic variation in Alzheimer’s disease (AD) brain is currently unclear.
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ORIGIN-PD enables rational enrichment for NLRP3/NF-κB inhibitor trials by identifying patients with inflammatory involvement.
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Individuals with comparable Alzheimer’s disease (AD) pathology can differ markedly in cognition, but the molecular nature of this heterogeneity remains unclear.
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Endolysosomal dysfunction is a central feature of many neurodegenerative disorders.
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16/100
Late-life depression (LLD) is increasingly recognized as a complex multisystem disorder associated with accelerated biological aging, impaired physiological resilience, frailty, and an increased risk of cognitive decline and dementia.
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These findings identify conserved regulatory networks that may contribute to female-biased microglial responses to AD pathology across mice and humans.
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Structured metabolic genetic axes reveal selective and biologically distinct links between circulating metabolism and neurodegenerative disease, providing a framework for mechanism-focused follow-up beyond single-metabolite association.
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Auditory dysfunction can precede clinical dementia, but the molecular progression of Alzheimer disease (AD) pathology from the sensory periphery to auditory cortex remains poorly resolved.
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Alzheimer’s disease (AD) is a widely prevalent neurodegenerative disorder characterized by progressive cognitive impairment and neuropathological alterations.
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Capturing the systemic effects of drugs in vivo remains a fundamental challenge for drug repurposing strategies.
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These findings demonstrate that Tau deletion induces an active, multilevel gain-of-resilience rather than passive resistance.
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Based on the exacerbated AD pathological features and transcriptomic alterations observed in Arf4 knockdown animals, ARF4 appears to play a critical role in AD resilience and may represent a potential prognostic factor worthy of further investigation.
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Genome-wide association studies have identified nearly 100 genetic loci that affect Alzheimer’s disease risk.
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This study investigated volumetric MRI differences of the thalamic nuclei in asymptomatic young adult C9orf72 expansion carriers compared to non-carriers, and examined spatial associations with normative thalamic transcriptomics from 8 weeks post-conception through middle age.
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In the present analysis, genetic risk and end-stage AD pathology are largely decoupled at the level of individual genes and pathways but converge on a shared, pharmacologically modifiable response landscape.
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The reproducibility crisis in biomedical research calls for re-evaluation of how common analytic approaches affect results.
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Whether the nodal vulnerability in dementia is solely represented by changes in cellular abundance or attrition of cellular transcriptomic landscape attribute to that transition in aging brain is yet to uncover with minutiae.
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16/100
Aging muscle showed increased inflammatory, extracellular-matrix, and stromal communication programs.
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These findings identify restoration of hippocampal transcript fate and splice-isoform selection as a mechanism potentially underlying A. muciniphila -mediated protection against Cd neurotoxicity, and establish post-transcriptional RNA regulation as a gut-brain target for mitigating environmentally driven neurotoxicity.
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Many biological quantities in omics are inherently periodic or directional, including circadian phase, cell-cycle position, and cellular orientation.
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Single-cell RNA sequencing (scRNA-seq) studies of Alzheimer’s disease (AD) mouse models have proliferated across independent laboratories, brain regions, and platforms, yet the cross-study reproducibility of transcriptional signatures derived from such data remains underexplored.
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Frontotemporal lobar degeneration (FTLD), predominantly comprised of tau and TDP-43 proteinopathies, is a common cause of early-onset dementia.
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Postmitotic neurons must preserve genome integrity for decades despite continuous oxidative, transcription-associated, and environmental DNA damage.
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Synapse loss is the strongest pathological correlate of cognitive decline in Alzheimer’s disease, yet the molecular basis of synaptic vulnerability across disease progression remains poorly understood.
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Cerebrospinal fluid (CSF) contains brain derived proteins that can be leveraged as biomarkers for Alzheimer’s disease (AD) and other neurodegenerative diseases.
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We then integrated healthy retinal expression, AD retinal proteomics, and PD aqueous-humor proteomics with the brain-concordance results.
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16/100
Severe cognitive decline due to dementia is an important clinical indicator signaling neurodegeneration.
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Genetic studies have identified thousands of variants associated with brain-related traits.
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Formalin-fixed, paraffin-embedded (FFPE) brain tissue is a major archival resource, yet its suitability for high-density DNA methylation profiling is limited by fixation-induced DNA fragmentation and crosslinking.
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MicroRNAs (miRNAs) are implicated in Alzheimer's disease (AD), but research has focused on individual miRNAs and direct targets.
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Immunofluorescence staining of FFPE tissue following Xenium processing also preserves cellular morphology, allowing the morphological complexity of distinct cell types to be captured and quantitated, especially for glial cells with highly ramified processes.
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Familial Alzheimer’s disease (fAD) is an early-onset form of AD caused by autosomal-dominant variants in APP, PSEN1, or PSEN2, with PSEN1 accounting for most genetically defined cases [1].
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TAR DNA-binding protein 43 (TDP-43) is a key pathological hallmark of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) and a critical regulator of RNA splicing.
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Nuclear depletion of TDP-43 is a defining pathological feature of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), leading to widespread RNA misprocessing, including the formation of cryptic exons.
From across this tag
9 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 9. The same 9 appear here every time.
- A shared disease-associated oligodendrocyte signature among multiple CNS pathologies
- MicroRNA predicts cognitive performance in healthy older adults
- Identification of miRNA changes in Alzheimer's disease brain and CSF yields putative biomarkers and insights into disease pathways
- Large-scale deep proteomic analysis in Alzheimer's disease brain regions across race and ethnicity
- Epigenetic changes in Alzheimer's disease: decrements in DNA methylation
- Integrative multi-omic profiling of adult mouse brain endothelial cells and potential implications in Alzheimer's disease
- Genome-wide association meta-analysis identifies 48 risk variants and highlights the role of the stria vascularis in hearing loss
- SCAN: Spatiotemporal Cloud Atlas for Neural cells
- DNA Methylation in Alzheimer's Disease