ArticleFrontiers in aging neuroscience2022
Accelerated aging-related transcriptome alterations in neurovascular unit cells in the brain of Alzheimer's disease.
Article in Frontiers in aging neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Integrative genomics and single-cell CRISPRi screening dissect Alzheimer GWAS non-coding variants regulating TSPAN14.American journal of human genetics · 2026Article
- CSF proteomic profiling with amyloid and tau pathology identifies distinctive sex-specific alteration of multiple proteins involved in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Comparative Multi-Omics Analysis Identifies Shared Transcriptomic Signatures and Therapeutic Targets in Alzheimer's, Parkinson's, and Huntington's Diseases.Current issues in molecular biology · 2025Article
- Article
- Machine-learning based strategy identifies a robust protein biomarker panel for Alzheimer's disease in cerebrospinal fluid.Alzheimer's research & therapy · 2025Article
- Integration of Single-Cell and Spatial Transcriptomic Data Reveals Spatial Architecture and Potential Biomarkers in Alzheimer's Disease.Molecular neurobiology · 2025Article
- An Update on Neuroaging on Earth and in Spaceflight.International journal of molecular sciences · 2025Review
- Deciphering motor dysfunction and microglial activation in mThy1-Frontiers in molecular neuroscience · 2025Article
- Neuroinflammaging: A Tight Line Between Normal Aging and Age-Related Neurodegenerative Disorders.Aging and disease · 2024Review
- Using blood transcriptome analysis for Alzheimer's disease diagnosis and patient stratification.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- A novel aging-associated lncRNA signature for predicting prognosis in osteosarcoma.Scientific reports · 2024Article
- Cell-type brain-region specific changes in prefrontal cortex of a mouse model of alcohol dependence.Neurobiology of disease · 2024Article
- Human isogenic cells of the neurovascular unit exert transcriptomic cell type-specific effects on a blood-brain barrier in vitro model of late-onset Alzheimer disease.Fluids and barriers of the CNS · 2023Article
- Review
- Longitudinal APOE4- and amyloid-dependent changes in the blood transcriptome in cognitively intact older adults.Alzheimer's research & therapy · 2023Article
- Review
- Review
- Targeting IGF1R signaling for brain aging and Alzheimer's disease.Aging pathobiology and therapeutics · 2022Article
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3 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common cause of dementia with no effective therapies. Aging is a dominant risk factor for AD. The neurovascular unit (NVU) plays an important role in maintaining homeostasis of the brain microenvironment. The accelerated aging of NVU cells may directly impair NVU function and contribute to AD pathogenesis. However, the expression patterns of aging-related genes (AGs) in NVU cells of AD remain unclear. In this study, we performed single-nucleus transcriptome analysis of 61,768 nuclei from prefrontal cortical samples of patients with AD and normal control (NC) subjects. Eight main cell types were identified, including astrocytes, microglia, excitatory neurons, inhibitory neurons, oligodendrocytes, oligodendrocyte precursor cells, pericytes, and endothelial cells. Transcriptomic analysis identified the expression patterns of AGs in NVU cells of AD. Gene set enrichment analysis confirmed the key aging-associated cellular pathways enriched in microglia and oligodendrocytes. These aging-related transcriptomic changes in NVU were cross-validated using bulk transcriptome data. The least absolute shrinkage and selection operator regression method was used to select the crucial AGs most associated with AD: IGF1R, MXI1, RB1, PPARA, NFE2L2, STAT5B, FOS, PRKCD, YWHAZ, HTT, MAPK9, HSPA9, SDHC, PRKDC, and PDPK1. This 15-gene model performed well in discriminating AD from NC samples. Among them, IGF1R, MXI1, PPARA, YWHAZ, and MAPK9 strongly correlated with pathologic progression in AD, were identified as critical regulators of AD. Although most AGs showed similar trends of expression changes in different types of NVU cells in AD, certain AGs were expressed in a cell-specific manner. Our comprehensive analysis of brain NVU from patients with AD reveals previously unknown molecular changes associated with aging that may underlie the functional dysregulation of NVU, providing important insights for exploring potential cell-specific therapeutic targets to restore brain homeostasis in AD.
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