ArticleBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2025
Identification of novel small molecule chaperone activators for neurodegenerative disease treatment.
Article in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
- Heat Shock Protein 90: From Molecular Chaperone Function to Therapeutic Targeting in Malignancies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Holding but not folding: How a single charge flip uncouples the DNAJC7-Hsp70 relay in amyotrophic lateral sclerosis.The FEBS journal · 2026Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A pathological hallmark of neurodegenerative disease is the accumulation of aberrant protein aggregates which contribute to the cytotoxicity and are therefore a target for therapy development. One key mechanism to manage cellular protein homeostasis is heat shock proteins (HSPs), protein chaperones which are known to target aberrant protein accumulation. Activation of HSPs target aberrant TDP-43, tau and amyloid to rescue neurodegenerative disease. As an attempt to target HSP activation for neurodegeneration therapy, we here develop a drug screening assay to identify compounds that will activate the master regulator of HSPs, the transcription factor heat shock factor 1 (HSF1). As HSF1 is bound by HSP90 which prevents its activation, we developed a NanoBRET assay, which allows us to monitor and quantify the HSF1-HSP90 interaction in living cells to screen for compounds disrupting this interaction and thereby releasing HSF1 for activation. After the optimisation and validation of the assay, a two thousand compound library was screened which produced 10 hits including two known HSP90 inhibitors. Follow-up functional study showed that one of the hits oxyphenbutazone (OPB) significantly reduces the accumulation of insoluble TDP-43 in a cell model, eliciting no signs of stress or toxicity. Overall, this study demonstrates a viable strategy for new drug discovery in targeting aberrant proteins and identifies potential candidates for translation into neurodegenerative disease treatment.
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Registered trials
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