ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2024
Proteomic changes in the human cerebrovasculature in Alzheimer's disease and related tauopathies linked to peripheral biomarkers in plasma and cerebrospinal fluid.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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38 citing papers in PubMed.
- Collagen Triple Helix Repeat Containing 1 (CTHRC1) in the Nervous System: Expression, Signaling Mechanisms, and Functional Implications.Journal of molecular neuroscience : MN · 2026Review
- Semaphorin 3G (SEMA3G) is a highly selective marker of cerebral amyloid angiopathy.bioRxiv : the preprint server for biology · 2026Article
- VINE-seq and MultiVINE-seq for single-nucleus and multiome profiling of the brain vasculature.Nature protocols · 2026Review
- The emerging roles of ITM2A: At the molecular crossroads of development and pathogenesis.iScience · 2026Review
- Deep Plasma Proteomics-Based Diagnostic Panel for Early Detection of Amnestic Mild Cognitive Impairment.Journal of proteome research · 2026Article
- Cerebrovascular Single-Nucleus RNA-Seq Reveals Heat Shock Activation and Vascular Remodeling in Alzheimer's Disease and Primary Tauopathies.Research square · 2026Article
- Polyol pathway dysregulation in CSF links glucose metabolism to tau pathology independently of amyloid and genetic predisposition.medRxiv : the preprint server for health sciences · 2026Article
- Early syndecan-4 upregulation predicts cognitive and pathological trajectories in Alzheimer disease.Alzheimer's research & therapy · 2026Article
- Proteomic signatures of the APOE ε4 and APOE ε2 genetic variants and Alzheimer's disease.Nature aging · 2026Article
- PSEN1 mutant marmoset fibroblasts mimic multi-omic signatures of Alzheimer's disease.bioRxiv : the preprint server for biology · 2026Article
- The Amyloid Plaque Proteomes of Alzheimer's Disease and Mild Cognitive Impairment.Research square · 2026Article
- Plasma Proteomic Analysis ofmedRxiv : the preprint server for health sciences · 2026Article
- A fully iPS-cell-derived 3D model of the human blood-brain barrier for exploring neurovascular disease mechanisms and therapeutic interventions.Nature neuroscience · 2026Article
- Assessing Aβ-independent effects of Module 42 on immune function in vitro.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Plasma proteomics reveals molecular overlap between physical activity and dementia risk.Brain communications · 2026Article
- Electroacupuncture Prevents Against AD-Like Phenotypes in APP/PS1 Mice: Investigation of the Mechanisms From Cerebral Microangiopathy.CNS neuroscience & therapeutics · 2025Article
- Molecular profiling of brain endothelial cell to astrocyte endfoot communication in mouse and human.Nature communications · 2025Article
- Neuronal gene profiling of tau oligomer-bearing cholinergic nucleus basalis neurons during the onset of Alzheimer's disease.Acta neuropathologica communications · 2025Article
- Multi-scale integration of human brain vascular and CSF proteomes reveals biomarkers of cerebral amyloid angiopathy linked to Alzheimer's disease risk.medRxiv : the preprint server for health sciences · 2025Article
- Plasma proteomic associations with Alzheimer's disease endophenotypes.Nature aging · 2025Article
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Abstract
introductionCerebrovascular dysfunction is a pathological hallmark of Alzheimer's disease (AD). Nevertheless, detecting cerebrovascular changes within bulk tissues has limited our ability to characterize proteomic alterations from less abundant cell types.
methodsWe conducted quantitative proteomics on bulk brain tissues and isolated cerebrovasculature from the same individuals, encompassing control (N = 28), progressive supranuclear palsy (PSP) (N = 18), and AD (N = 21) cases.
resultsProtein co-expression network analysis identified unique cerebrovascular modules significantly correlated with amyloid plaques, cerebrovascular amyloid angiopathy (CAA), and/or tau pathology. The protein products within AD genetic risk loci were concentrated within cerebrovascular modules. The overlap between differentially abundant proteins in AD cerebrospinal fluid (CSF) and plasma with cerebrovascular network highlighted a significant increase of matrisome proteins, SMOC1 and SMOC2, in CSF, plasma, and brain. DISCUSSION: These findings enhance our understanding of cerebrovascular deficits in AD, shedding light on potential biomarkers associated with CAA and vascular dysfunction in neurodegenerative diseases.
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