ArticleJournal of biomedical science2024
Targeting cathepsin S promotes activation of OLF1-BDNF/TrkB axis to enhance cognitive function.
Article in Journal of biomedical science, 2024. 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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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.
- Bidirectional causal association between cathepsins and neuropsychiatric disorders: univariate and multivariate Mendelian randomization study.European archives of psychiatry and clinical neuroscience · 2026Article
- The promising role of cathepsins as biomarkers and therapeutic targets in glioblastoma.Discover oncology · 2026Review
- DNAH11 impairs memory via disrupted synaptic plasticity in noise-induced hidden hearing loss mice.Cell biology and toxicology · 2025Article
- Protein co-aggregates of dense core amyloid plaques and CSF differ in rapidly progressive Alzheimer's disease and slower sporadic Alzheimer's disease.Alzheimer's research & therapy · 2025Article
- From Synaptic Plasticity to Neurodegeneration: BDNF as a Transformative Target in Medicine.International journal of molecular sciences · 2025Review
- Cordycepin combined with antioxidant effects improves fatigue caused by excessive exercise.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
backgroundCathepsin S (CTSS) is a cysteine protease that played diverse roles in immunity, tumor metastasis, aging and other pathological alterations. At the cellular level, increased CTSS levels have been associated with the secretion of pro-inflammatory cytokines and disrupted the homeostasis of Ca
methodsWe conducted classic Y-maze and Barnes Maze tests to assess the spatial and working memory of Ctss
resultsOur findings reported that targeting cathepsin S (CTSS) yields improvements in cognitive function, enhancing both working and spatial memory in behavior models. Ex vivo studies showed elevated levels of long-term potentiation levels and increased synaptic complexity. Microarray analysis demonstrated that brain-derived neurotrophic factor (BDNF) was upregulated when CTSS was knocked down by using siRNA. Moreover, the pharmacological blockade of the CTSS enzymatic activity promoted BDNF expression in a dose- and time-dependent manner. Notably, the inhibition of CTSS was associated with increased neurogenesis in the murine dentate gyrus. These results suggested a promising role of CTSS modulation in cognitive enhancement and neurogenesis.
conclusionOur findings suggest a critical role of CTSS in the regulation of cognitive function by modulating the Ca
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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 Socratic graph.