ArticleFluids and barriers of the CNS2020
The microvascular extracellular matrix in brains with Alzheimer's disease neuropathologic change (ADNC) and cerebral amyloid angiopathy (CAA).
Article in Fluids and barriers of the CNS, 2020. 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, 31 citations in OpenAlex.
- TREM2 deficiency causes region-specific brain effects in a mouse model of cerebral amyloid angiopathy.bioRxiv : the preprint server for biology · 2026Article
- Spatially resolved transcriptomic profiling identifies distinct signatures in parenchymal and vascular microenvironments in Alzheimer's Disease with Cerebral Amyloid Angiopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Hyaluronic acid: emerging roles and biomaterial innovations in Alzheimer's and Parkinson's disease therapy.Frontiers in pharmacology · 2026Review
- Functions of the basal lamina and ApoE in cerebral amyloid angiopathy.Fluids and barriers of the CNS · 2025Review
- Microvascular Health as a Key Determinant of Organismal Aging.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Brain vascular basement membrane: Comparison of human and mouse brain at the transcriptomic and proteomic levels.Matrix biology : journal of the International Society for Matrix Biology · 2025Article
- Structural changes in cerebral microvasculature induced by ferroptosis contribute to blood-brain barrier disruption in Alzheimer's disease: an autopsy study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Plasma S100β is a predictor for pathology and cognitive decline in Alzheimer's disease.Fluids and barriers of the CNS · 2025Article
- Models and mechanisms of post-stroke dementia and cognitive impairment.Frontiers in stroke · 2025Article
- Loss of TREM2 diminishes CAA despite an overall increase of amyloid load in Tg-SwDI mice.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Challenges and Future Perspectives in Modeling Neurodegenerative Diseases Using Organ-on-a-Chip Technology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Integrated Systems Analysis Deciphers Transcriptome and Glycoproteome Links in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2024Article
- Revealing third-order interactions through the integration of machine learning and entropy methods in genomic studies.BioData mining · 2024Article
- The Brain and Spinal Microvasculature in Normal Aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023Review
- Article
- Tumor Necrosis Factor (TNF)-α-Stimulated Gene 6 (TSG-6): A Promising Immunomodulatory Target in Acute Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Matrix disequilibrium in Alzheimer's disease and conditions that increase Alzheimer's disease risk.Frontiers in neuroscience · 2023Review
- Enlarged Perivascular Spaces and Age-Related Clinical Diseases.Clinical interventions in aging · 2023Review
- Pathological changes within the cerebral vasculature in Alzheimer's disease: New perspectives.Brain pathology (Zurich, Switzerland) · 2022Review
- Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe microvasculature (MV) of brains with Alzheimer's disease neuropathologic change (ADNC) and cerebral amyloid angiopathy (CAA), in the absence of concurrent pathologies (e.g., infarctions, Lewy bodies), is incompletely understood.
objectiveTo analyze microvascular density, diameter and extracellular matrix (ECM) content in association with ADNC and CAA.
methodsWe examined samples of cerebral cortex and isolated brain microvasculature (MV) from subjects with the National Institute on Aging-Alzheimer's Association (NIA-AA) designations of not-, intermediate-, or high ADNC and from subjects with no CAA and moderate-severe CAA. Cases for all groups were selected with no major (territorial) strokes, ≤ 1 microinfarct in screening sections, and no Lewy body pathology. MV density and diameter were measured from cortical brain sections. Levels of basement membrane (BM) ECM components, the protein product of TNF-stimulated gene-6 (TSG-6), and the ubiquitous glycosaminoglycan hyaluronan (HA) were assayed by western blots or HA ELISA of MV lysates.
resultsWe found no significant changes in MV density or diameter among any of the groups. Levels of BM laminin and collagen IV (col IV) were lower in MV isolated from the high ADNC vs. not-ADNC groups. In contrast, BM laminin was significantly higher in MV from the moderate-severe CAA vs. the no CAA groups. TSG-6 and HA content were higher in the presence of both high ADNC and CAA, whereas levels of BM fibronectin and perlecan were similar among all groups.
conclusionsCortical MV density and diameter are not appreciably altered by ADNC or CAA. TSG-6 and HA are increased in both ADNC and CAA, with laminin and col IV decreased in the BM of high ADNC, but laminin increased in moderate-severe CAA. These results show that changes in the ECM occur in AD and CAA, but independently of one another, and likely reflect on the regional functioning of the brain microvasculature.
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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 OpenQuestion graph.