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Blood-brain barrier (BBB) breakdown, due to the concomitant disruption of the tight junctions (TJs), normally required for the maintenance of BBB function, and to the altered transport of molecules between blood and brain and vice-versa, has been suggested to significantly contribute to the development and progression of different brain disorders including Huntington's disease (HD). Although the detrimental consequence the BBB breakdown may have in the clinical settings, the timing of its alteration remains elusive for many neurodegenerative diseases. In this study we demonstrate for the first time that BBB disruption in HD is not confined to established symptoms, but occurs early in the disease progression. Despite the obvious signs of impaired BBB permeability were only detectable in concomitance with the onset of the disease, signs of deranged TJs integrity occur precociously in the disease and precede the onset of overt symptoms. To our perspective this finding may add a new dimension to the horizons of pathological mechanisms underlying this devastating disease, however much remains to be elucidated for understanding how specific BBB drug targets can be approached in the future.
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http://dx.doi.org/10.1038/srep41316 | DOI Listing |
Mol Cell Neurosci
September 2025
Department of Personalized & Molecular Medicine, Era University, Lucknow, India.
Epilepsy is a neurological disorder that shows strong genetic control on the timing and onset of symptoms and drug response variability. Some epilepsy syndromes have clear monogenic mutations but genes with control on the phenotype and severity of the disorder and drug sensitivity are present in the whole genetic profile. Genetic modifiers are not the cause of epilepsy but control significant networks such as synaptic plasticity and ion channels and neurodevelopment and neuroinflammation and therefore the reason why two individuals with the same primary mutations have different clinical courses.
View Article and Find Full Text PDFEur J Pharm Sci
September 2025
Department of Neurology, Massachusetts General Hospital, Boston, MA, 02129, USA; Neuroscience Program, Harvard Medical School, Boston, MA, 02129, USA. Electronic address:
Glioblastoma (GBM) is a highly malignant brain tumor with limited treatment options and poor prognosis. GBM exhibits resistance to conventional therapies, including temozolomide (TMZ), radiotherapy, and immunotherapy, partly due to immunosuppressive mechanisms such as programmed death-ligand 1 (PD-L1) overexpression. To address these challenges, we developed TMZ-loaded nanostructured lipid carriers (NLCs) conjugated with anti-PD-L1 single-chain variable fragments (scFv) for dual chemo-immunotherapy.
View Article and Find Full Text PDFJ Biol Chem
September 2025
Institute of Anatomy and Cell Biology, University of Würzburg, Würzburg, Germany. Electronic address:
WNT7A and WNT7B, secreted by neural cells, are essential regulators of developmental brain angiogenesis and blood-brain barrier integrity. In brain endothelial cells, WNT7 proteins activate β-catenin signaling through the ligand-specific receptor complex GPR124-RECK and classical WNT receptors of the FZD and LRP families. Previous studies suggested that WNT7 isoforms assemble a GPR124-RECK-FZD-LRP5/6 multi-receptor complex for signaling.
View Article and Find Full Text PDFBioorg Chem
September 2025
Department of Pharmacy, Personalized Drug Research and Therapy Key Laboratory of Sichuan Province, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China. Electronic address:
RET tyrosine kinase, a key regulator of cellular signaling, is abnormally activated due to mutations or fusions in various cancers, making it an important therapeutic target. Traditional multi-kinase inhibitors (MKIs, such as cabozantinib and vandetanib) exhibit significant side effects due to non-selective inhibition of targets like VEGFR, and also suffer from resistance associated with RET mutations (e.g.
View Article and Find Full Text PDFJ Am Chem Soc
September 2025
College of Medical Engineering, Beijing Institute of Technology, 6 Jinfeng Road, Zhuhai, 519088, China.
Multiple biological barriers severely restrict the delivery efficiency of nanoparticles (NPs) to tumors. To overcome biological barriers, traditional NPs usually require a complex design, which increases the difficulty of clinical translation. Therefore, there appears to be a dilemma between the complex biological barriers and clinical requirement for a simple molecular structure of NPs.
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