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Nanodiagnosis and Treatment System for Human Health

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Nanoscience".

Deadline for manuscript submissions: 20 June 2026 | Viewed by 1870

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Key Laboratory of Polyoxometalate and Reticular Material Chemistry of Ministry of Education and Faculty of Chemistry, Northeast Normal University, Changchun, China
Interests: chirality
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Special Issue Information

Dear Colleagues,

In recent years, nanodiagnostic and therapeutic systems have shown great potential in the diagnosis and treatment of human diseases. In terms of disease diagnosis, nanotechnology provides more accurate tools for medical imaging, such as using nanoparticle contrast agents, which can significantly improve the resolution and specificity of medical imaging. Nanosensor and nanoprobe technology have also been applied to the detection of biomolecules, achieving early detection and precise diagnosis of diseases. Furthermore, nanodrugs are constantly emerging, and anti-tumor drugs, such as Abraxane (Bristol Myers Squibb), Nb457 (HIV nano-antibody), and even lipid nanoparticle (LNP) delivery systems used in mRNA vaccines, have begun to significantly improve human health. Despite facing numerous challenges at present, we still look forward to the broader application prospects of nanodiagnosis and treatment systems. Since this Special Issue belongs to IJMS, all research article submissions should involve research at the molecular level as well as verified experiments.

Prof. Dr. Nan Gao
Guest Editor

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Keywords

  • nanodiagnosis
  • nanodrugs
  • nano-antibody
  • nanosensor
  • nanoprobe technology

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Published Papers (2 papers)

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Research

22 pages, 9081 KB  
Article
Hydrophobic Drug Delivery Platforms Based on Covalent Organic Frameworks for Combined Treatment of Alzheimer’s Disease
by Yun Zhao, Ziwei Wang, Enpeng Xi, Fuming Yang and Nan Gao
Int. J. Mol. Sci. 2025, 26(21), 10803; https://doi.org/10.3390/ijms262110803 - 6 Nov 2025
Viewed by 531
Abstract
Alzheimer’s disease (AD) is a complex neurodegenerative disease. The pathogenesis of AD remains incompletely understood. It is characterized by a variety of neuropathological changes, including neuroinflammation, neuronal loss and synaptic damage. Multiple pathological changes make achieving good therapeutic effects with a single drug [...] Read more.
Alzheimer’s disease (AD) is a complex neurodegenerative disease. The pathogenesis of AD remains incompletely understood. It is characterized by a variety of neuropathological changes, including neuroinflammation, neuronal loss and synaptic damage. Multiple pathological changes make achieving good therapeutic effects with a single drug treatment difficult, and using multiple drugs for combination therapy is currently the most effective method. Currently, the mainstay drugs used for AD treatment are hydrophobic drugs, such as curcumin, donepezil, and resveratrol. Because hydrophobic drugs cannot dissolve in bodily fluids and often aggregate or precipitate, their efficacy is greatly reduced. Therefore, there is an urgent need for a drug carrier that can effectively load and continuously release drugs. However, currently, there are few drug carriers that can achieve efficient co-loading of multiple hydrophobic drugs. Therefore, three of two-dimensional imine covalent organic frameworks (COFs) with different monomers were synthesized through rational design and screening. These three synthesized COFs are simultaneously loaded with curcumin (CUR) and benzofurazan (BZ) to achieve combined therapy. The results indicate that among this series of synthesized COFs, the COF synthesized from 4,4′,4″-(1,3,5-Triazine-2,4,6-triyl) trianiline and benzene-1,3,5-tricarboxaldehyde (COF-TB) exhibits optimal hydrophobic drug-loading capacity, enabling effective co-loading of CUR and BZ (BC@COF-TB). After treatment with BC@COF-TB, the cognitive function of 5×FAD mice was significantly improved. The COF platform provides a new way to deliver hydrophobic drugs for AD treatment. Full article
(This article belongs to the Special Issue Nanodiagnosis and Treatment System for Human Health)
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25 pages, 4746 KB  
Article
Neurotrophic and Neurotoxic Effects of Aβ42 and Its Oligomers on Neuronal Survival: Revealed by Their Opposite Influence on the Potency of Extracellular BDNF
by He Li, Changxin Zheng, Kai Wen, Tianyu Zhang and Yingjiu Zhang
Int. J. Mol. Sci. 2025, 26(10), 4501; https://doi.org/10.3390/ijms26104501 - 8 May 2025
Viewed by 1016
Abstract
Brain-derived neurotrophic factor (BDNF) is critical for neuronal survival. Amyloid-β monomers (Aβ42M) and oligomers (Aβ42O) have trophic and toxic effects on neuronal survival, respectively. Branched oligosaccharides (BOs) and catechins (CAs) can specifically bind to Aβ42M/Aβ42O, influencing both effects. However, whether and how Aβ42M/Aβ42O [...] Read more.
Brain-derived neurotrophic factor (BDNF) is critical for neuronal survival. Amyloid-β monomers (Aβ42M) and oligomers (Aβ42O) have trophic and toxic effects on neuronal survival, respectively. Branched oligosaccharides (BOs) and catechins (CAs) can specifically bind to Aβ42M/Aβ42O, influencing both effects. However, whether and how Aβ42M/Aβ42O influences BDNF remains unknown. This study investigated the interaction between Aβ42M/Aβ42O and BDNF, the effects of Aβ42M and Aβ42O on BDNF binding to the TrkB/p75 receptor and their impact on BDNF-supported cell survival, and the roles of BOs and CAs in these processes. BDNF exhibited stronger binding affinity for Aβ42M and Aβ42O than BOs/CAs. Aβ42M increased neuronal viability by synergistically enhancing BDNF binding to TrkB and p75, whereas Aβ42O decreased neuronal viability by inactivating/consuming BDNF, thereby reducing its binding to these receptors. BDNF-Aβ42O binding appeared to mutually neutralize/counteract each other’s biological effects; therefore, increasing BDNF levels might reduce Aβ42O’s neurotoxicity. By competitively targeting Aβ42M/Aβ42O rather than BDNF or its receptors, BOs and CAs enhanced these effects. These findings suggest that Aβ42M’s neurotrophicity was directly linked to its synergistic enhancement of BDNF activity, whereas Aβ42O’s neurotoxicity was primarily due to its inactivation or consumption of BDNF. This study provided valuable insights for developing BOs/CAs-based neuroprotective therapeutics or nanomaterials against AD. Full article
(This article belongs to the Special Issue Nanodiagnosis and Treatment System for Human Health)
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