ArticleThe Journal of biological chemistry2017
A mechanistic model to predict effects of cathepsin B and cystatin C on β-amyloid aggregation and degradation.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 18 citations in OpenAlex.
- Cathepsin B prevents cell death by fragmentation and destruction of pathological amyloid fibrils.Cell death discovery · 2025Article
- Monocytes release cystatin F dimer to associate with Aβ and aggravate amyloid pathology and cognitive deficits in Alzheimer's disease.Journal of neuroinflammation · 2024Article
- Effect of Ovocystatin on Amyloid β 1-42 Aggregation-In Vitro Studies.International journal of molecular sciences · 2023Article
- Regulatory role of cathepsin L in induction of nuclear laminopathy in Alzheimer's disease.Aging cell · 2022Article
- Serum Cystatin C Predicts Stroke Clinical Outcomes at 1 Year Independent of Renal Function.Frontiers in neurology · 2021Article
- Chronic Periodontitis and Alzheimer Disease: A Putative Link of Serum Proteins Identification by 2D-DIGE Proteomics.Frontiers in aging neuroscience · 2020Article
- Association of cathepsin B and cystatin C with an age-related pulmonary subclinical state in a healthy Chinese population.Therapeutic advances in respiratory diseaseArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
β-Amyloid (Aβ) aggregation is thought to initiate a cascade of neurodegenerative events in Alzheimer's disease (AD). Much effort is underway to develop strategies to reduce Aβ concentration or inhibit aggregation. Cathepsin B (CatB) proteolytically degrades Aβ into non-aggregating fragments but is potently inhibited by cystatin C (CysC). It has been suggested that decreasing CysC would facilitate Aβ clearance by relieving CatB inhibition. However, CysC binds Aβ and inhibits Aβ aggregation, suggesting that an intervention that increases CysC would prevent Aβ aggregation. Both approaches have been tested in animal models, yielding contradictory results, possibly because of the opposing influences of CysC on Aβ degradation
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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.