ReviewActa neuropathologica2024
The contribution of β-amyloid, Tau and α-synuclein to blood-brain barrier damage in neurodegenerative disorders.
Review in Acta neuropathologica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
45 citing papers in PubMed, 57 citations in OpenAlex.
- The Dual Roles of Extracellular Vesicle Subtypes in Regulating Traumatic Brain Injury.International journal of molecular sciences · 2026Review
- The vicious cycle: unraveling the interplay between α-synuclein, mitochondrial dysfunction, and neuroinflammation in Parkinson's disease.Journal of neurology · 2026Review
- Glycolysis: The Bridge Between Cellular Interaction and Alzheimer's Disease.Biomolecules · 2026Review
- von Willebrand Factor fibers formed at pathological high shear provide a scaffold for α-synuclein binding and aggregation.Scientific reports · 2026Article
- Toxic Alpha-Synuclein and the Opening of the Gate: Blood-Brain Barrier Damage and Stepwise Leukocyte Infiltration.Cellular and molecular neurobiology · 2026Review
- Neurovascular Uncoupling in Alzheimer's and Parkinson's Diseases: Mechanisms and Therapeutic Strategies.Brain sciences · 2026Review
- A Meta-analysis to Identify Common Key Genes Across Ageing, Alzheimer's and Parkinson's Diseases.Annals of neurosciences · 2026Article
- Hypertension as a Major Risk Factor in Alzheimer's Disease: Mechanisms, Interactions and Therapeutic Perspectives.Clinical interventions in aging · 2026Review
- The prognostic potential of circulating BDNF levels and its polymorphisms in age-related cognitive impairment and neurodegeneration.Frontiers in aging neuroscience · 2026Review
- Blood-brain Barrier Dysfunction in Parkinson's Disease: Mechanisms and Emerging Therapeutic Strategies.Current neurovascular research · 2026Review
- Long-term LDL cholesterol burden and stroke: mechanistic insights and emerging strategies for personalized lipid management.Frontiers in neurology · 2026Review
- Hyaluronic acid: emerging roles and biomaterial innovations in Alzheimer's and Parkinson's disease therapy.Frontiers in pharmacology · 2026Review
- Emerging pathological mechanisms of Alzheimer's disease pathogenesis: from neuroimmune interactions to intercellular communication.Frontiers in aging neuroscience · 2026Review
- MRI-DTI contributes to evaluating diffuse neural injury following repetitive mild traumatic brain injury.iScience · 2025Article
- Article
- Multiple Mechanisms and Therapeutic Strategies for the Involvement of AMPK in the Development of Alzheimer's Disease.Molecular neurobiology · 2025Review
- Tau mediates the impact of amyloid and vascular disease burden on the trajectory of clinical symptoms.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Microbial Metabolomes in Alzheimer's Disease: From Pathogenesis to Therapeutic Potential.Current issues in molecular biology · 2025Review
- Adherence to an anti-inflammatory diet is associated with lower Alzheimer's disease mortality: A modifiable risk factor in a national cohort.The journal of prevention of Alzheimer's disease · 2025Article
- The Cerebral Lymphatic System: Function, Controversies, and Therapeutic Approaches for Central Nervous System Diseases.Cellular and molecular neurobiology · 2025Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Central nervous system (CNS) accumulation of fibrillary deposits made of Amyloid β (Aβ), hyperphosphorylated Tau or α-synuclein (α-syn), present either alone or in the form of mixed pathology, characterizes the most common neurodegenerative diseases (NDDs) as well as the aging brain. Compelling evidence supports that acute neurological disorders, such as traumatic brain injury (TBI) and stroke, are also accompanied by increased deposition of toxic Aβ, Tau and α-syn species. While the contribution of these pathological proteins to neurodegeneration has been experimentally ascertained, the cellular and molecular mechanisms driving Aβ, Tau and α-syn-related brain damage remain to be fully clarified. In the last few years, studies have shown that Aβ, Tau and α-syn may contribute to neurodegeneration also by inducing and/or promoting blood-brain barrier (BBB) disruption. These pathological proteins can affect BBB integrity either directly by affecting key BBB components such as pericytes and endothelial cells (ECs) or indirectly, by promoting brain macrophages activation and dysfunction. Here, we summarize and critically discuss key findings showing how Aβ, Tau and α-syn can contribute to BBB damage in most common NDDs, TBI and stroke. We also highlight the need for a deeper characterization of the role of these pathological proteins in the activation and dysfunction of brain macrophages, pericytes and ECs to improve diagnosis and treatment of acute and chronic neurological disorders.
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.