ArticleActa neuropathologica communications2019
Apolipoprotein E and clusterin inhibit the early phase of amyloid-β aggregation in an in vitro model of cerebral amyloid angiopathy.
Article in Acta neuropathologica communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Suppression of neuronal eEF2K alleviates cognitive deficits and apathy-like behavior in APP/PS1 AD model mice.Research square · 2026Article
- The complement cascade in Alzheimer's disease: modern implications of an ancient immune protagonist.Molecular neurodegeneration · 2025Review
- Deciphering the role of APOE in cerebral amyloid angiopathy: from genetic insights to therapeutic horizons.Annals of medicine · 2025Review
- Intrahippocampally Injected Human Recombinant Clusterin Reduces Amyloid-β Aggregate Size in Cerebral Arteriole Walls of Clusterin Knockout Mice.Neuropathology and applied neurobiology · 2025Article
- An explorative analysis of plasma biomarkers associated with cerebral amyloid angiopathy.medRxiv : the preprint server for health sciences · 2025Article
- From Lab Bench to Hope: Emerging Gene Therapies in Clinical Trials for Alzheimer's Disease.Molecular neurobiology · 2025Review
- Capillary basal lamina in human brain and spinal cord has fibrillar collagen type I and type III: Ignorance may not be bliss.Free neuropathology · 2025Article
- Cerebral Proteomic Changes in the rTg-D Rat Model of Cerebral Amyloid Angiopathy Type-2 With Cortical Microhemorrhages and Cognitive Impairments.Neuroscience insights · 2024Article
- Molecular modeling of apoE in complexes with Alzheimer's amyloid-β fibrils from human brain suggests a structural basis for apolipoprotein co-deposition with amyloids.Cellular and molecular life sciences : CMLS · 2023Article
- The emerging role of the HTRA1 protease in brain microvascular disease.Frontiers in dementia · 2023Review
- Review
- Proteomic profiling in cerebral amyloid angiopathy reveals an overlap with CADASIL highlighting accumulation of HTRA1 and its substrates.Acta neuropathologica communications · 2022Article
- Overlapping Protein Accumulation Profiles of CADASIL and CAA: Is There a Common Mechanism Driving Cerebral Small-Vessel Disease?The American journal of pathology · 2021Review
- Structural basis of soluble membrane attack complex packaging for clearance.Nature communications · 2021Article
- MFG-E8 (LACTADHERIN): a novel marker associated with cerebral amyloid angiopathy.Acta neuropathologica communications · 2021Article
- Current Management and Therapeutic Strategies for Cerebral Amyloid Angiopathy.International journal of molecular sciences · 2021Review
- Comprehensive Identification of Potential Crucial Genes and miRNA-mRNA Regulatory Networks in Papillary Thyroid Cancer.BioMed research international · 2021Article
- The Role of HDL and HDL Mimetic Peptides as Potential Therapeutics for Alzheimer's Disease.Biomolecules · 2020Review
- Genetic architecture of common non-Alzheimer's disease dementias.Neurobiology of disease · 2020Review
- Understanding the Pathophysiology of Cerebral Amyloid Angiopathy.International journal of molecular sciences · 2020Review
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Sporadic cerebral amyloid angiopathy (CAA) is characterized by cerebrovascular amyloid-β (Aβ) deposition, which leads to lobar hemorrhage and dementia. Biological molecules affecting the development of CAA have not been fully characterized. In this study, we performed proteome analysis of biopsied leptomeningeal and cortical vessels obtained from 6 CAA patients and 5 non-CAA patients who underwent surgery for large lobar hemorrhages. We found that 6 proteins, including Aβ, apolipoprotein E (apoE), clusterin (CLU), albumin, complement C4 and vitronectin were significantly upregulated in the vessels of CAA patients as compared to non-CAA patients. ApoE and CLU were found in all CAA patients. We next examined the effects of apoE and CLU on the early phase of Aβ aggregation, using a simple yet powerful in vitro model of CAA, which recapitulates the intramural periarterial drainage pathway model. We found that physiological concentrations of apoE and CLU delayed the initiation time of amyloid growth kinetics in a concentration-dependent manner. These data indicate that apoE and CLU may act as extracellular chaperones to inhibit Aβ amyloid deposition in CAA.
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