ArticleFrontiers in aging neuroscience2020
Differential Profile of Systemic Extracellular Vesicles From Sporadic and Familial Alzheimer's Disease Leads to Neuroglial and Endothelial Cell Degeneration.
Article in Frontiers in aging neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Utilisation of Machine Learning Approaches Improves RNA-Seq Transcriptome Analyses in Alzheimer's Disease Brain.Journal of molecular neuroscience : MN · 2026Article
- Plasma extracellular vesicles and phosphorylated tau 181 as early biomarkers of cognitive impairment in Alzheimer's dementia.Alzheimer's research & therapy · 2026Article
- Aβ Modulates Extracellular Vesicles Proteomic Profile Impacting Phosphorylation Mediators.Molecular neurobiology · 2025Article
- Crosstalk Between Mitochondrial DNA and Immune Response: Focus on Autism Spectrum Disorder.Molecular neurobiology · 2025Review
- Driving research on successful aging and neuroprotection in Latin America: Insights from the inaugural symposium on brain resilience and healthy longevity.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Extracellular vesicles: biological mechanisms and emerging therapeutic opportunities in neurodegenerative diseases.Translational neurodegeneration · 2024Review
- siRNA drug delivery across the blood-brain barrier in Alzheimer's disease.Advanced drug delivery reviews · 2023Review
- The Tricky Connection between Extracellular Vesicles and Mitochondria in Inflammatory-Related Diseases.International journal of molecular sciences · 2023Review
- Gliovascular alterations in sporadic and familial Alzheimer's disease: APOE3 Christchurch homozygote glioprotection.Brain pathology (Zurich, Switzerland) · 2023Article
- Biomarker and therapeutic potential of peripheral extracellular vesicles in Alzheimer's disease.Advanced drug delivery reviews · 2022Review
- Engineering extracellular vesicles for Alzheimer's disease: An emerging cell-free approach for earlier diagnosis and treatment.WIREs mechanisms of disease · 2022Review
- Mitochondrial Extracellular Vesicles in CNS Disorders: New Frontiers in Understanding the Neurological Disorders of the Brain.Frontiers in molecular biosciences · 2022Review
- Extracellular Vesicles From 3xTg-AD Mouse and Alzheimer's Disease Patient Astrocytes Impair Neuroglial and Vascular Components.Frontiers in aging neuroscience · 2021Article
- Targeting CDK5 in Astrocytes Promotes Calcium Homeostasis Under Excitotoxic Conditions.Frontiers in cellular neuroscience · 2021Article
- Blood-Brain Barrier Breakdown: An Emerging Biomarker of Cognitive Impairment in Normal Aging and Dementia.Frontiers in neuroscience · 2021Review
- Beta-Secretase 1 Underlies Reactive Astrocytes and Endothelial Disruption in Neurodegeneration.Frontiers in cellular neuroscience · 2021Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Evidence suggests that extracellular vesicles (EVs) act as mediators and biomarkers of neurodegenerative diseases. Two distinct forms of Alzheimer disease (AD) are known: a late-onset sporadic form (SAD) and an early-onset familial form (FAD). Recently, neurovascular dysfunction and altered systemic immunological components have been linked to AD neurodegeneration. Therefore, we characterized systemic-EVs from postmortem SAD and FAD patients and evaluated their effects on neuroglial and endothelial cells. We found increase CLN-5 spots with vesicular morphology in the abluminal portion of vessels from SAD patients. Both forms of AD were associated with larger and more numerous systemic EVs. Specifically, SAD patients showed an increase in endothelial- and leukocyte-derived EVs containing mitochondria; in contrast, FAD patients showed an increase in platelet-derived EVs. We detected a differential protein composition for SAD- and FAD-EVs associated with the coagulation cascade, inflammation, and lipid-carbohydrate metabolism. Using mono- and cocultures (endothelium-astrocytes-neurons) and human cortical organoids, we showed that AD-EVs induced cytotoxicity. Both forms of AD featured decreased neuronal branches area and astrocytic hyperreactivity, but SAD-EVs led to greater endothelial detrimental effects than FAD-EVs. In addition, FAD- and SAD-EVs affected calcium dynamics in a cortical organoid model. Our findings indicate that the phenotype of systemic AD-EVs is differentially defined by the etiopathology of the disease (SAD or FAD), which results in a differential alteration of the NVU cells implied in neurodegeneration.
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