ArticleEuropean journal of medicinal chemistry2014
Identification of human presequence protease (hPreP) agonists for the treatment of Alzheimer's disease.
Article in European journal of medicinal chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 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.
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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
9 citing papers in PubMed, 34 citations in OpenAlex.
- Sustainable Synthesis of 1,2-Disubstituted Benzimidazoles as Promising α-Glucosidase Inhibitors: In Vitro and In Silico Evaluation.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Interactions of amyloidogenic proteins with mitochondrial protein import machinery in aging-related neurodegenerative diseases.Frontiers in physiology · 2023Review
- Targeting whole body metabolism and mitochondrial bioenergetics in the drug development for Alzheimer's disease.Acta pharmaceutica Sinica. B · 2022Review
- Role of PITRM1 in Mitochondrial Dysfunction and Neurodegeneration.Biomedicines · 2021Review
- A Comprehensive Account on Recent Progress in Pharmacological Activities of Benzimidazole Derivatives.Frontiers in pharmacology · 2021Review
- Bioenergetics and translational metabolism: implications for genetics, physiology and precision medicine.Biological chemistry · 2019Review
- Reinvestigating the synthesis and efficacy of small benzimidazole derivatives as presequence protease enhancers.European journal of medicinal chemistry · 2019Article
- Conformational transition pathway of R308K mutant glucokinase in the presence of the glucokinase activator YNKGKA4.FEBS open bio · 2018Article
- Increased neuronal PreP activity reduces Aβ accumulation, attenuates neuroinflammation and improves mitochondrial and synaptic function in Alzheimer disease's mouse model.Human molecular genetics · 2015Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Amyloid-β (Aβ), a neurotoxic peptide, is linked to the onset of Alzheimer's disease (AD). Increased Aβ content within neuronal cell mitochondria is a pathological feature in both human and mouse models with AD. This accumulation of Aβ within the mitochondrial landscape perpetuates increased free radical production and activation of the apoptotic pathway. Human Presequence Protease (hPreP) is responsible for the degradation of mitochondrial amyloid-β peptide in human neuronal cells, and is thus an attractive target to increase the proteolysis of Aβ. Therefore, it offers a potential target for Alzheimer's drug design, by identifying potential activators of hPreP. We applied structure-based drug design, combined with experimental methodologies to investigate the ability of various compounds to enhance hPreP proteolytic activity. Compounds 3c &4c enhanced hPreP-mediated proteolysis of Aβ (1-42), pF₁β (2-54) and fluorogenic-substrate V. These results suggest that activation of hPreP by small benzimidazole derivatives provide a promising avenue for AD treatment.
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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.