ArticleAlzheimer's & dementia (New York, N. Y.)2020
Caveolae, CD109, and endothelial cells as targets for treating Alzheimer's disease.
Article in Alzheimer's & dementia (New York, N. Y.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 9 citations in OpenAlex.
- Article
- Nanotechnology to Overcome Blood-Brain Barrier Permeability and Damage in Neurodegenerative Diseases.Pharmaceutics · 2025Review
- Thinking outside the black box: are the brain endothelial cells the new main target in Alzheimer's disease?Neural regeneration research · 2023Review
- Smooth muscle αEuropean heart journal open · 2023Article
- Review
- Caveolae, CD109, and endothelial cells as targets for treating Alzheimer's disease.Alzheimer's & dementia (New York, N. Y.) · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reduced functionality of transforming growth factor β (TGF-β) is a major pathogenetic component of Alzheimer's disease (AD). The reduction is caused by an ≈50% decrease in the AD brain of the TGF-β receptor, TGFBR, causing a bottleneck effect that reduces the downstream actions of TGF-β, which is highly disadvantageous for brain function. Degradation of TGFBR occurs in caveolae with participation by caveolin-1 (Cav-1) and CD109. Mechanisms for this are discussed. In the cerebral microcirculation, endothelial cells (which are rich in caveolae) carry CD109 as a surface marker that co-precipitates with Cav-1. Atorvastatin reduced Cav-1 by 75% and, because Cav-1 and CD109 co-immunoprecipitate reciprocally, atorvastatin would also reduce the level of CD109. Administration of atorvastatin as a component of combination therapy would diminish the degradation of TGFBR and thereby benefit patients with AD.
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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.