ArticleBioengineering & translational medicine2026
Neuron-targeted 2-deoxyglucose-dendrimer-rosiglitazone nanotherapy mitigates neuroinflammation and cognitive deficits in pediatric traumatic brain injury.
Article in Bioengineering & translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- 2-Deoxyglucose Dendrimer-Enabled Niclosamide Delivery to FRβ-Expressing Macrophages Alleviates Endometriosis Progression and Associated Hyperalgesia.Advanced healthcare materials · 2026Article
- Article
- 2-Deoxyglucose dendrimer-enabled niclosamide delivery to FRβ-expressing macrophages alleviates endometriosis progression and associated hyperalgesia.bioRxiv : the preprint server for biology · 2026Article
- Sex- and cell type-specific effects of dexmedetomidine on ferroptosis in neurons and microglia following traumatic brain injury in juvenile mice.Molecular neurobiology · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
Traumatic brain injury (TBI) remains a major global health challenge, characterized by high morbidity and mortality rates. Despite advances in neuroscience, the blood-brain barrier (BBB) limits the effectiveness of potential neuroprotective treatments. Recent nanotechnology breakthroughs have led to smart drug delivery systems that can cross the BBB and target injured brain areas. However, achieving the specificity needed to deliver therapies to affected neurons remains a challenge. In previous work, we developed a mixed-layered dendrimer functionalized with 2-deoxyglucose (2DG-D) for selective neuronal drug delivery. In this study, we explore the therapeutic potential of rosiglitazone (Rosi) for pediatric TBI by creating a 2DG-D-Rosi nanosystem, where Rosi is conjugated to 2DG-D to improve its solubility, bioavailability, and targeted delivery to injured neurons. In vitro, 2DG-D-Rosi demonstrated high neuronal uptake, sustained drug release, and excellent biocompatibility. It significantly reduced neuronal apoptosis, reactive oxygen species formation, pro-inflammatory cytokine expression, and caspase activity, outperforming free Rosi. In vivo, using a pediatric TBI mouse model, 2DG-D-Rosi improved neuronal targeting, reduced neuroinflammation, and enhanced behavioral outcomes. This research highlights 2DG-D-Rosi as a promising nanotherapeutic platform for precise TBI treatment and sets the stage for developing more effective therapies for this challenging condition.
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