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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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Genome-wide association studies (GWAS) have identified many loci that contribute to the risk of neurodegenerative diseases.
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Alzheimer's disease (AD) is characterized by the deposition of amyloid-beta (Aβ) and microtubule-associated protein tau (MAPT) neurofibrillary tangles in the brain; however, the molecular mechanisms underlying associated synaptic dysfunction remain unclear.
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Alzheimer’s disease (AD) is characterised by aberrant amyloid beta and tau aggregation, neuroinflammation, demyelination and neurodegeneration, which have been linked to changes in cell-specific gene expression signatures.
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16/100
Frontotemporal dementia (FTD) caused by progranulin (GRN) mutations is associated with pronounced thalamic degeneration, yet the cellular basis of selective thalamic vulnerability remains poorly understood.
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The Amaryllidaceae geophyte Lycoris radiata is a primary botanical source of high-value medicinal alkaloids, including the Alzheimer’s therapeutic galanthamine.
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Validated on synthetic ground truth, the audit separates a generalizable anchor (PTGDS) from a dataset-specific signal and a global-expression artefact, providing a reusable control for trajectory-based molecular staging.
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These findings implicate significant liver–brain crosstalk through which chronic alcohol exposure may modulate AD-relevant pathology and reinforce the growing recognition of the liver as a critical organ in AD pathogenesis.
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Lysosomal dysfunction in myeloid cells is increasingly implicated in neurodegenerative diseases.
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Neurodegenerative diseases are a major threat to older adults and represent a growing global health burden as the elderly population continues to expand.
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These findings shift AD modeling from passive proteotoxicity to an active, misregulated developmental structural engine, offering a mechanical framework that explains early olfactory vulnerability and non-linear anti-tau clinical trial responses.
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The retina displayed earlier and broader AD-related molecular alterations than the hippocampus.
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IKZF1 is prioritised as a candidate late-disease microglial TF, supported by six convergent evidence dimensions including independent bulk replication.
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Lipid-processing microglia are among the microglial states most strongly associated with Alzheimer’s disease (AD) pathology, yet whether this association reproduces across independent cohorts, what transcriptional programs define the state, and which upstream signals and small molecules can modulate it remain unsolved.
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Aberrant alternative splicing alters multiple disease-associated splicing events, including MAPT exon 10 inclusion linked to tau pathology, and thereby impacts Alzheimer’s disease (AD) progression.
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Long non-coding RNAs (lncRNAs) are increasingly recognized as regulators of brain cell function, but their roles in astrocyte biology and neurodegeneration remain poorly understood.
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Alzheimer's disease (AD) is not an inevitable outcome of pathology but a dynamic process shaped by how brain cells respond to amyloid-β (Aβ) and tau.
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Down syndrome (DS), caused by trisomy 21, confers a near-universal risk for Alzheimer’s disease (AD), yet individuals exhibit marked variability in cognitive decline, suggesting the presence of cellular mechanisms that modulate vulnerability and resilience.
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48/100
Microglia are central mediators of neuroinflammation in Alzheimer's disease (AD), yet conserved microglial states and activation trajectories across AD mouse models remain incompletely defined.
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Amyloid plaques contain numerous proteins in addition to amyloid beta in Alzheimer’s disease (AD).
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The existence of human hippocampal neurogenesis has long been disputed1-12 and its relevance in cognition remains unknown.
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Three AD subtypes were identified. Subtype 1, enriched in RNA metabolism pathways, showed the mildest atrophy and slowest cognitive decline.
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Our comprehensive atlas revealed pronounced heterogeneity among microglial states, with disease-associated microglia (DAM) significantly enriched in AD brains compared to controls.
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Major depressive disorder (MDD) is linked to a higher risk of premature aging, but the mechanisms underlying this association remain unclear.
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Nine female-specific associations were identified and replicated, involving ADGRV1, OR3A3, IFI27L1, LYRM1, STAP2, TSTD2, PDYN, and TMEM50B. We observed the preponderance of protective female-specific associations in neurons.
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43/100
The cerebellum, essential for motor coordination and increasingly recognized for its role in cognition, is typically considered more resilient to aging and largely spared from hallmark Alzheimer's disease (AD) pathology.
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Spatial biology technologies enable high-dimensional profiling within intact tissues, revealing how molecular and cellular organization drives function and disease.
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43/100
The study of transcriptomic and epigenomic variations in neurodegenerative diseases, particularly tauopathies like Pick's disease (PiD) and Alzheimer's disease (AD), offers insights into their underlying regulatory mechanisms.
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Subjective cognitive decline (SCD) is widely regarded as a potential preclinical stage of Alzheimer's disease (AD), yet its genetic basis remains poorly understood.
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43/100
Somatic mutations are DNA sequence changes that occur in non-reproductive cells during an organism's life and are not inherited by offspring.
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Transcriptomics and polygenic risk analysis position resilience as an intermediate AD state.
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16/100
Alzheimer's disease (AD) is the most common neurodegenerative disorder, yet the molecular mechanisms underlying its region- and cell-type-specific pathogenesis remain poorly defined.
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MicroRNA dysregulation is implicated in neurodegenerative disorders, including Alzheimer’s disease (AD).
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Aging represents a major risk for human neurodegenerative disorders, such as dementia and Alzheimer's disease, and is associated with a functional decline in neurons and impaired synaptic plasticity, leading to a gradual decline in memory.
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Temporal lobe epilepsy (TLE) is the most common and drug-resistant type of epilepsy with an unknown mechanism.
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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline, yet its epigenetic underpinnings remain elusive.
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Cerebrovascular dysfunction underlies many neurological disorders, yet how genetic variants in brain vascular cells drive disease risk remains unknown.
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Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder characterized by heterogeneous molecular changes across diverse cell types, posing significant challenges for treatment development.
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Circular RNAs (circRNAs) are emerging as a promising object of study in Alzheimer's disease (AD) pathogenesis.
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Exercise's protective effects in Alzheimer's disease (AD) are well recognized, but cell-specific contributions to this phenomenon remain unclear.
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Both neuronal and peripheral tissues become disrupted in Alzheimer's disease (AD).
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We employed Stereo-seq combined with single-nucleus RNA sequencing (snRNA-seq) to investigate the gene expression and cell composition changes in human hippocampus with or without Alzheimer's disease (AD).
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The integrated stress response (ISR) is a highly conserved network essential for maintaining cellular homeostasis and cognitive function.
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43/100
Alzheimer's disease (AD) is a progressive neurodegenerative disorder with profound global impact.
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We identified common disease endotypes, such as dedifferentiation, dysregulation of synaptic signaling, repression of mitochondrial function and metabolism, and inflammation.
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To date, DNA methylation is the best characterized epigenetic modification in Alzheimer's disease.
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The ability to accurately quantify biological age could help monitor and control healthy aging.
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Single-nucleus RNA-sequencing (snRNA-seq) has revealed new levels of cellular organization and diversity within the human brain.
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The same vulnerable inhibitory neuron subtype was depleted in both AD and DLB.
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The pathogenesis of Alzheimer's disease (AD) depends on environmental and heritable factors, with its molecular etiology still unclear.
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Single-nucleus transcriptomic studies have revealed glial cell states associated with Alzheimer's disease; however, these nuclei are dissociated from the complex architecture of the human neocortex.
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.
- Large-scale deep multi-layer analysis of Alzheimer's disease brain reveals strong proteomic disease-related changes not observed at the RNA level
- Epigenetic Regulation in Neurodegenerative Diseases
- A History of Repeated Alcohol Intoxication Promotes Cognitive Impairment and Gene Expression Signatures of Disease Progression in the 3xTg Mouse Model of Alzheimer's Disease
- Brain expression quantitative trait locus and network analyses reveal downstream effects and putative drivers for brain-related diseases
- A coordinated and reproducible multicellular response to AD pathology
- TDP-43 dysfunction induces cryptic circular RNAs in ALS/FTD
- Single-nucleus transcriptional profiling uncovers the reprogrammed metabolism of astrocytes in Alzheimer's disease
- Recent advances in the application of metabolomics to Alzheimer's Disease
- Gene expression profiling of 12633 genes in Alzheimer hippocampal CA1: transcription and neurotrophic factor down-regulation and up-regulation of apoptotic and pro-inflammatory signaling