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single-cell
274 studies tagged single-cell, 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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Dementia and cognitive disorders are major aging-associated pathologies.
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Oligodendrocyte dysfunction has been implicated in the pathogenesis of neurodegenerative diseases, so understanding oligodendrocyte activation states would shed light on disease processes.
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Immature dentate granule cells (imGCs) arising from adult hippocampal neurogenesis contribute to plasticity and unique brain functions in rodents 1,2 and are dysregulated in multiple human neurological disorders 3-5 .
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Alzheimer's disease (AD) is a complex neurodegenerative disease, perturbing neuronal and non-neuronal cell populations.
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Cortical neuron loss is a pathological hallmark of late-onset Alzheimer's disease (AD).
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Epigenetic age has emerged as an important biomarker of biological ageing.
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Therapeutics based on short interfering RNAs (siRNAs) delivered to hepatocytes have been approved, but new delivery solutions are needed to target additional organs.
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Hearing loss is one of the top contributors to years lived with disability and is a risk factor for dementia.
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Dementia in Alzheimer's disease progresses alongside neurodegeneration 1-4 , but the specific events that cause neuronal dysfunction and death remain poorly understood.
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Resolving glial contributions to Alzheimer's disease (AD) is necessary because changes in neuronal function, such as reduced synaptic density, altered electrophysiological properties, and degeneration, are not entirely cell autonomous.
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Alzheimer's disease (AD) is the most common form of dementia, characterized by progressive cognitive impairment and neurodegeneration.
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Alzheimer's disease (AD) is the most common neurodegenerative disease, with cognitive decline as the primary clinical feature.
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The biological processes that are disrupted in the Alzheimer's disease (AD) brain remain incompletely understood.
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We identified several DEGs in both neuronal and glial cell subtypes in comparisons of wild type (WT) versus 5XFAD and WT versus T2KO mice, including Ttr, Fth1, Pcsk1n, Malat1, Rpl37, Rtn1, Sepw1, Uba52, Mbp, Arl6ip5, Gm26917, Vwa1, and Pgrmc1.
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The hippocampal-entorhinal system supports cognitive functions, has lifelong neurogenic capabilities in many species, and is selectively vulnerable to Alzheimer's disease.
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43/100
Single-cell RNA sequencing (scRNA-seq) distinguishes cell types, states and lineages within the context of heterogeneous tissues.
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In recent decades, our understanding of the molecular changes involved in neurodegenerative diseases has been transformed.
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The neocortex is disproportionately expanded in human compared with mouse 1,2 , both in its total volume relative to subcortical structures and in the proportion occupied by supragranular layers composed of neurons that selectively make connections within the neocortex and with other telencephalic structures.
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83/100
Mass spectrometry-based proteomics empowers deep profiling of proteome and protein posttranslational modifications (PTMs) in Alzheimer's disease (AD).
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43/100
Alzheimer's disease (AD) is characterized by extracellular aggregates of amyloid β peptides, intraneuronal tau aggregates, and neuronal death.
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Understanding the tissue-specific genetic controls of protein levels is essential to uncover mechanisms of post-transcriptional gene regulation.
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43/100
The gene-regulatory landscape of the brain is highly dynamic in health and disease, coordinating a menagerie of biological processes across distinct cell types.
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Microglia, the tissue-resident macrophages of the central nervous system (CNS), play critical roles in immune defense, development and homeostasis.
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59/100
Sporadic Alzheimer's disease (AD) exclusively affects elderly people.
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Single-cell RNA-sequencing (scRNA-Seq) is widely used to reveal the heterogeneity and dynamics of tissues, organisms, and complex diseases, but its analyses still suffer from multiple grand challenges, including the sequencing sparsity and complex differential patterns in gene expression.
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Genome-wide association studies (GWAS) have identified more than 40 loci associated with Alzheimer's disease (AD), but the causal variants, regulatory elements, genes and pathways remain largely unknown, impeding a mechanistic understanding of AD pathogenesis.
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Novel therapeutic strategies for Alzheimer's disease (AD) are of the greatest priority given the consistent failure of recent clinical trials focused on Aβ or pTau.
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In this issue of Neuron, Wang et al. employ an impressive multi-omics approach, including gene co-expression network analyses and drug repositioning, to normalize disease-disrupted gene modules and identify a therapeutically relevant driver of Alzheimer's disease.
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Alzheimer's disease (AD) is characterized by the selective vulnerability of specific neuronal populations, the molecular signatures of which are largely unknown.
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Previous studies showed that U1 small nuclear RNA (snRNA) was selectively enriched in the brain of individuals with familial Alzheimer's disease (AD), resulting in widespread changes in RNA splicing.
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There was no difference in age acceleration between dementia cases and controls.
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50/100
PS2V levels increased in AD postmortem brain but PS2V was also present at significant levels in FTD and LBD brains.
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45/100
The extent of microglial heterogeneity in humans remains a central yet poorly explored question in light of the development of therapies targeting this cell type.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder of the brain and the most common form of dementia among the elderly.
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Genome-wide association studies of neurological diseases have identified thousands of variants associated with disease phenotypes.
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Alzheimer's disease (AD) lacks protein biomarkers reflective of its diverse underlying pathophysiology, hindering diagnostic and therapeutic advancements.
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39/100
Alzheimer's disease (AD) is a devastating neurological disorder characterized by changes in cell-type proportions and consequently marked alterations of the transcriptome.
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Protein aggregation is the hallmark of neurodegeneration, but the molecular mechanisms underlying late-onset Alzheimer's disease (AD) are unclear.
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Alzheimer's disease (AD) is the most common form of dementia but has no effective treatment.
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43/100
The repeated failures of amyloid-targeting therapies have challenged our narrow understanding of Alzheimer's disease (AD) pathogenesis and inspired wide-ranging investigations into the underlying mechanisms of disease.
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39/100
The past decade has seen the maturation of multiple different forms of high-dimensional molecular profiling to the point that these methods could be deployed in initially hundreds and more recently thousands of human samples.
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41/100
Single-nucleus RNA sequencing (snRNA-seq) is used as an alternative to single-cell RNA-seq, as it allows transcriptomic profiling of frozen tissue.
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We describe a human single-nuclei transcriptomic atlas for the substantia nigra (SN), generated by sequencing approximately 17,000 nuclei from matched cortical and SN samples.
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The expression of microRNA (miRNA) is influenced by ongoing biological processes, including aging, and has begun to play a role in the measurement of neurodegenerative processes in central nervous system.
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Our results demonstrate that novel AD biomarker candidates are identified and confirmed by proteomic studies of brain tissue and biofluids, providing a rich resource for large-scale biomarker validation for the AD community.
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Although complex inflammatory-like alterations are observed around the amyloid plaques of Alzheimer's disease (AD), little is known about the molecular changes and cellular interactions that characterize this response.
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Psychiatric disorders are associated with accelerated aging and enhanced risk for neurodegenerative disorders.
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Alzheimer's disease is a progressive neurodegenerative disorder, with the strongest disease-associated changes observed at clinical or end-stage disease.
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Damage-associated microglia (DAM) profiles observed in Alzheimer's disease (AD)-related mouse models reflect an activation state that could modulate AD risk or progression.
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Aetiological and clinical heterogeneity is increasingly recognized as a common characteristic of Alzheimer's disease and related dementias.
From across this tag
7 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 7. The same 7 appear here every time.
- HOP-1, a Caenorhabditis elegans presenilin, appears to be functionally redundant with SEL-12 presenilin and to facilitate LIN-12 and GLP-1 signaling
- Transcription Factor-Wide Association Studies to Identify Functional SNPs in Alzheimer's Disease
- Deep proteomic network analysis of Alzheimer's disease brain reveals alterations in RNA binding proteins and RNA splicing associated with disease
- Astrocyte transcriptomic changes along the spatiotemporal progression of Alzheimer's disease
- Multi-omic atlas of the parahippocampal gyrus in Alzheimer's disease
- Long Non-coding RNA BACE1-AS May Serve as an Alzheimer's Disease Blood-Based Biomarker
- Phenotype Scoring of Population Scale Single-Cell Data Dissects Alzheimer's Disease Complexity