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single-nucleus
274 studies tagged single-nucleus, 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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The role of non-neuronal cells in Alzheimer's disease progression has not been fully elucidated.
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Our understanding of Alzheimer's disease (AD) pathophysiology remains incomplete.
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Recent research efforts provided compelling evidence of genome-wide DNA methylation alterations in aging and age-related disease.
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Numerous clinical trials of drug candidates for Alzheimer's disease (AD) have failed, and computational drug repositioning approaches using omics data have been proposed as effective alternative approaches to the discovery of drug candidates.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder that mostly strikes the elderly.
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Alzheimer's disease is an incurable neurodegenerative disorder in which neuroinflammation has a critical function 1 .
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38/100
Alzheimer's disease (AD) displays a long asymptomatic stage before dementia.
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There is currently little information available about how individual cell types contribute to Alzheimer's disease.
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Noncoding genetic variation is a major driver of phenotypic diversity, but functional interpretation is challenging.
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Alzheimer's disease (AD) is the most common neurodegenerative disorder causing huge emotional and economic burden to our societies.
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Circulating long noncoding RNAs (lncRNAs) might serve as biomarkers for different pathological conditions.
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We devise a conceptually different computational framework based on a holistic view, where single-cell datasets are used to infer global, large-scale regulatory networks.
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Epigenetic control of enhancers alters neuronal functions and may be involved in Alzheimer's disease (AD).
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The biological markers of aging used to predict physical health status in older people are of great interest.
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Epigenetic influence of brain and neuronal function plays key regulatory roles in health and diseases.
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Further analysis of the AD brain proteome will continue to yield new insights into the biological basis of AD.
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Alzheimer's disease (AD) affects half the US population over the age of 85 and is universally fatal following an average course of 10 years of progressive cognitive disability.
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We initiated the systematic profiling of the dorsolateral prefrontal cortex obtained from a subset of autopsied individuals enrolled in the Religious Orders Study (ROS) or the Rush Memory and Aging Project (MAP), which are jointly designed prospective studies of aging and dementia with detailed, longitudinal cognitive phenotyping during life and a quantitative, structured neuropathologic examination after death.
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41/100
Alzheimer's disease (AD) is an age-associated neurodegenerative disease characterized by amyloidosis, tauopathy, and activation of microglia, the brain resident innate immune cells.
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Investigators have long suspected that pathogenic microbes might contribute to the onset and progression of Alzheimer's disease (AD) although definitive evidence has not been presented.
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Mechanisms of epigenetic regulation, including DNA methylation, chromatin remodeling, and histone post-translational modifications, are involved in multiple aspects of neuronal function and development.
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Identifying reliable biomarkers of aging is a major goal in geroscience.
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48/100
Patients with Alzheimer's disease (AD) and Parkinson's disease (PD) often have overlap in clinical presentation and brain neuropathology suggesting that these two diseases share common underlying mechanisms.
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Aging is the strongest risk factor for Alzheimer's disease (AD), although the underlying mechanisms remain unclear.
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Progress toward the development of efficacious therapies for Alzheimer's disease (AD) is halted by a lack of understanding early underlying pathological mechanisms.
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Recent genome-wide association studies (GWAS) have identified numerous genetic risk variants for late-onset Alzheimer's disease (AD) and Parkinson's disease (PD).
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Circular RNAs (circRNAs) represent a special group of noncoding single-stranded highly stable ribonucleic acid entities abundant in the eukaryotic transcriptome.
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Microglia, the CNS-resident immune cells, play important roles in disease, but the spectrum of their possible activation states is not well understood.
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Microglia, the tissue-resident macrophages in the brain, are damage sensors that react to nearly any perturbation, including neurodegenerative diseases such as Alzheimer's disease (AD).
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Early expression disturbance of hub genes is an important feature of AD development, and interfering with this process may reverse the disease progression.
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MicroRNAs are small non-coding RNAs that function as regulators of gene expression.
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Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized in the early stages by loss of learning and memory.
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Here, we report proteomic analyses of 129 human cortical tissues to define changes associated with the asymptomatic and symptomatic stages of Alzheimer's disease (AD).
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Differential correlation analysis, a bioinformatics tool to elucidate complicated and interdependent biological systems behind diseases, detects effective MCI markers that cannot be found by single molecule analysis such as t-test.
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Our understanding of the highly specialized functions for small non-coding single-stranded RNA (ssRNA) in the transcriptome of the human central nervous system (CNS) continues to evolve.
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This transcriptomic network analysis of 19 brain regions provides a comprehensive assessment of the critical molecular pathways associated with AD pathology and offers new insights into molecular mechanisms underlying selective regional vulnerability to AD at different stages of the progression of cognitive compromise and development of the canonical neuropathological lesions of AD.
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Previous genome-wide association studies (GWAS), conducted by our group and others, have identified loci that harbor risk variants for neurodegenerative diseases, including Alzheimer's disease (AD).
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Small ubiquitin-like modifiers (SUMOs) are essential for the regulation of several cellular processes and are potential therapeutic targets owing to their involvement in diseases such as cancer and Alzheimer disease.
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A common approach to understanding neurodegenerative disease is comparing gene expression in diseased versus healthy tissues.
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The cell types that trigger the primary pathology in many brain diseases remain largely unknown.
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We have characterized changes in DNA methylation in the superior temporal gyrus of patients with Alzheimer's disease, highlighting novel loci that facilitate better characterization of pathways and mechanisms underlying Alzheimer's disease pathogenesis, and improve our understanding of epigenetic signatures that may contribute to the development of disease.
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There is an urgent need to develop molecular biomarkers of brain age in order to advance our understanding of age related neurodegeneration.
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One hundred and fifty probe-sets form an accurate classifier of young versus older muscle tissue and this healthy ageing RNA classifier performed consistently in independent cohorts of human muscle, skin and brain tissue (n = 594, AUC = 0.83-0.96) and thus represents a biomarker for biological age.
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Alarming epidemiological features of Alzheimer's disease impose curative treatment rather than symptomatic relief.
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Epigenetics is a quickly growing field encompassing mechanisms regulating gene expression that do not involve changes in the genotype.
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Drug repositioning offers an innovative approach to drug discovery with great potential in the field of Alzheimer's Disease and dementia therapeutics.
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Alzheimer's disease (AD) is a severe age-related neurodegenerative disorder characterized by accumulation of amyloid-β plaques and neurofibrillary tangles, synaptic and neuronal loss, and cognitive decline.
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There is no consensus for a blood-based test for the early diagnosis of Alzheimer's disease (AD).
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52/100
We used a collection of 708 prospectively collected autopsied brains to assess the methylation state of the brain's DNA in relation to Alzheimer's disease (AD).
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DNA methylation (5-methylcytosine [5mC]) is one of several epigenetic markers altered in Alzheimer's disease (AD) brain.
From across this tag
10 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 10. The same 10 appear here every time.
- Age-Associated Transcriptomic and Epigenetic Alterations in Mouse Hippocampus
- High-Dimensional Multi-Omic Mapping of Post-Mortem Human Brain Using Iterative Indirect Immunofluorescence Imaging on Xenium-Processed Tissues
- Multi-Omic analyses characterize the ceramide/sphingomyelin pathway as a therapeutic target in Alzheimer's disease
- MicroRNA predicts cognitive performance in healthy older adults
- Whole transcriptome sequencing reveals gene expression and splicing differences in brain regions affected by Alzheimer's disease
- Identification of miRNA changes in Alzheimer's disease brain and CSF yields putative biomarkers and insights into disease pathways
- Integrating CSF and EV Proteomes Enhances Biomarker Discovery by Capturing Shared Variation Across Compartments
- Methylation differences in Alzheimer's disease neuropathologic change in the aged human brain
- Proteomics analysis of plasma from middle-aged adults identifies protein markers of dementia risk in later life
- Proteomics reveals three molecular subtypes of Alzheimer's disease with distinct progression patterns