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The accurate prediction of neurotoxicity in peptides and proteins is essential for the safety evaluation of therapeutic proteins and genetically modified (GM) organisms. Existing tools, including our earlier method NTxPred, typically use a single predictive model for both neurotoxic peptides and proteins, despite their structural and functional differences. This lack of specialization may lead to suboptimal performance and limited generalizability. To address this, we developed NTxPred2, distinct, specialized models for predicting neurotoxic peptides and neurotoxins (proteins). Our curated datasets include 877 neurotoxic and 877 non-toxic peptides, and 775 neurotoxic and 775 non-toxic proteins. Certain residues, like cysteine, are prevalent in both but in different magnitudes. Using composition and binary profiles, our machine-learning models achieved an area under the curve (AUC) of 0.97 for peptides and 0.85 for proteins, improving to 0.89 with evolutionary information. Models using protein embeddings reached 0.96 AUC for peptides and 0.94 for proteins, while protein language models achieved 0.98 (esm2-t30) and 0.91 (esm2-t6). All models were validated via five-fold cross-validation, and the final models were evaluated on an independent dataset. We further assessed protein models on the peptide dataset and vice versa, highlighting the necessity of separate models. The proposed models outperform existing methods on independent datasets that are not used for training. Our neurotoxicity prediction models will aid in the safety assessment of GM foods and therapeutic proteins by minimizing the need for animal testing. To support the scientific community, we developed a standalone software and web server NTxPred2 for predicting and scanning neurotoxins (https://webs.iiitd.edu.in/raghava/ntxpred2/, https://github.com/raghavagps/ntxpred2/).
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http://dx.doi.org/10.1002/pro.70200 | DOI Listing |
Gen Physiol Biophys
September 2025
Department of Neurology, Hubei Third People's Hospital of Jianghan University, Wuhan, China.
In this study, we investigated the therapeutic potential of calycosin (from Astragalus) in Alzheimer's disease (AD), focusing on ferroptosis modulation. APP/PS1 mice received 40 mg/kg calycosin for 3 months. Cognitive function was assessed via Morris water maze test.
View Article and Find Full Text PDFNeuropharmacology
September 2025
Department of Pharmaceutical Sciences, School of Pharmacy, Massachusetts College of Pharmacy and Health Sciences, Boston, USA. Electronic address:
Gymnema sylvestre (G. sylvestre) is a traditional medicinal herb known for its anti-diabetic properties, yet its molecular mechanisms remain unknown. Growing evidence suggests a strong link between insulin resistance and neurodegeneration, mediated by impaired pro-survival signaling (e.
View Article and Find Full Text PDFCNS Neurosci Ther
September 2025
School of Public Health, Guangxi Medical University, Nanning, Guangxi, China.
Background: Lead (Pb) exposure is recognized for its contribution to the development of neurodegenerative diseases. However, the precise mechanisms underlying Pb-induced neurological dysfunction remain elusive. This study aimed to investigate the role of oxidative stress and the autophagy-related P62/kelch like ECH-associated protein 1 (Keap1)/Nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in neuronal impairment caused by Pb.
View Article and Find Full Text PDFSignal Transduct Target Ther
September 2025
State Key Laboratory of Advanced Medical Materials and Devices, Tianjin Key Laboratory of Radiation Medicine and Molecular Nuclear Medicine, Tianjin Institutes of Health Science, Institute of Radiation Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China. fans
Radiation-induced brain injury (RIBI) represents a severe complication of cranial radiotherapy, substantially diminishing patients' quality of life. Unlike conventional brain injuries, RIBI evokes a unique chronic neuroinflammatory response that notably aggravates neurodegenerative processes. Despite significant progress in understanding the molecular mechanisms related to neuroinflammation, the specific and precise mechanisms that regulate neuroinflammation in RIBI and its associated toxicological effects remain largely unclear.
View Article and Find Full Text PDFACS Chem Neurosci
September 2025
Computational Biology and Molecular Simulations Laboratory, Department of Biophysics, School of Medicine, Bahçeşehir University, Istanbul 34349, Turkey.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the pathological aggregation of amyloid-beta (Aβ) peptides, particularly Aβ-42, which plays a central role in disease progression. Soluble Aβ dimers have been implicated as the primary neurotoxic species contributing to synaptic dysfunction and cognitive impairment. In this study, we employ a comprehensive computational framework integrating molecular dynamics (MD) simulations, neural relational inference (NRI) modeling, and largest Lyapunov exponent (LLE) analysis to elucidate the molecular mechanisms underlying Aβ-42 dimerization and evaluate the inhibitory potential of small molecules, apigenin and caffeine.
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