ArticleNeuropathology and applied neurobiology2020
Brain mural cell loss in the parietal cortex in Alzheimer's disease correlates with cognitive decline and TDP-43 pathology.
Article in Neuropathology and applied neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- Reframing TDP-43 in Alzheimer's disease: From co-pathology to neurovascular culprit.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Reduced SUMOylation impairs NOTCH3 signaling and cell survival in the pathogenesis of CADASIL.Cell communication and signaling : CCS · 2025Article
- CD2AP at the junction of nephropathy and Alzheimer's disease.Molecular neurodegeneration · 2025Review
- Perivascular phosphorylated TDP-43 inclusions are associated with Alzheimer's disease pathology and loss of CD146 and Aquaporin-4.Brain pathology (Zurich, Switzerland) · 2025Article
- Lower GLUT1 and unchanged MCT1 in Alzheimer's disease cerebrovasculature.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- Limbic-predominant age-related TDP-43 encephalopathy (LATE-NC): Co-pathologies and genetic risk factors provide clues about pathogenesis.Journal of neuropathology and experimental neurology · 2024Review
- A high-throughput single-cell RNA expression profiling method identifies human pericyte markers.Neuropathology and applied neurobiology · 2023Article
- Research Progress on Natural Plant Molecules in Regulating the Blood-Brain Barrier in Alzheimer's Disease.Molecules (Basel, Switzerland) · 2023Review
- Higher angiotensin-converting enzyme 2 (ACE2) levels in the brain of individuals with Alzheimer's disease.Acta neuropathologica communications · 2023Article
- Limbic-predominant age-related TDP43 encephalopathy (LATE) neuropathological change in neurodegenerative diseases.Nature reviews. Neurology · 2023Review
- Direct and Indirect Effects of Filamin A on Tau Pathology in Neuronal Cells.Molecular neurobiology · 2023Article
- Higher Angiotensin I Converting Enzyme 2 (ACE2) levels in the brain of individuals with Alzheimer's disease.bioRxiv : the preprint server for biology · 2023Article
- Cerebrovascular insulin receptors are defective in Alzheimer's disease.Brain : a journal of neurology · 2023Article
- Pathological changes within the cerebral vasculature in Alzheimer's disease: New perspectives.Brain pathology (Zurich, Switzerland) · 2022Review
- Blood-brain barrier leakage in Alzheimer's disease: From discovery to clinical relevance.Pharmacology & therapeutics · 2022Review
- Effects of Cadmium Exposure on Leydig Cells and Blood Vessels in Mouse Testis.International journal of environmental research and public health · 2022Article
- Evidence of Filamin A loss of solubility at the prodromal stage of neuropathologically-defined Alzheimer's disease.Frontiers in aging neuroscience · 2022Article
- Peripheral Pathways to Neurovascular Unit Dysfunction, Cognitive Impairment, and Alzheimer's Disease.Frontiers in aging neuroscience · 2022Review
- Vascular pathology and pathogenesis of cognitive impairment and dementia in older adults.Cerebral circulation - cognition and behavior · 2022Article
- Role of Retinoid X Receptors (RXRs) and dietary vitamin A in Alzheimer's disease: Evidence from clinicopathological and preclinical studies.Neurobiology of disease · 2021Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
aimsBrain mural cells (BMC), smooth muscle cells and pericytes, interact closely with endothelial cells and modulate numerous cerebrovascular functions. A loss of BMC function is suspected to play a role in the pathophysiology of Alzheimer's Disease (AD).
methodsBMC markers, namely smooth muscle alpha actin (α-SMA) for smooth muscle cells, as well as platelet-derived growth factor receptor β (PDGFRβ) and aminopeptidase N (ANPEP or CD13) for pericytes, were assessed by Western immunoblotting in microvessel extracts from the parietal cortex of 60 participants of the Religious Orders study, with ages at death ranging from 75 to 98 years old.
resultsParticipants clinically diagnosed with AD had lower vascular levels of α-SMA, PDGFRβ and CD13. These reductions were correlated with lower cognitive scores for global cognition, episodic and semantic memory, perceptual speed and visuospatial ability. In addition, α-SMA, PDGFRβ and CD13 were negatively correlated with vascular Aβ40 concentrations. Vascular levels of BMC markers were also inversely correlated with insoluble cleaved phosphorylated transactive response DNA binding protein 43 (TDP-43) (25 kDa) and positively correlated with soluble cleaved phosphorylated TDP-43 (35 kDa) in cortical homogenates, suggesting strong association between BMC loss and cleaved phosphorylated TDP-43 aggregation.
conclusionsThe results of this study highlight a loss of BMC in AD. The associations between α-SMA, PDGFRβ and CD13 vascular levels with cognitive scores, TDP-43 aggregation and cerebrovascular accumulation of Aβ in the parietal cortex suggest that BMC loss contributes to both AD symptoms and pathology, further strengthening the link between cerebrovascular defects and dementia.
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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.