Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Alzheimer's disease (AD) affects 40 million individuals globally and is characterized by the accumulation of amyloid-beta (Aβ) proteins, which aggregate and form plaques. BBB dysfunction drives AD cerebrovascular pathology and BBB integrity is maintained by neurovascular unit (NVU). Specifically, within the NVU, the cerebral endothelial cells maintain vascular homeostasis. In this study, we isolated endothelial-enriched regions of interest (ROIs) using the Nanostring GeoMx digital spatial profiler and employed a deconvolution model to evaluate transcriptomic changes. We observed dysregulation of cellular signaling potentially disrupting the APP+ BBB integrity. Analysis of ligand-receptor pairings that are the foundation of the NVU intercellular signaling indicated that the endothelial vasculature completes a feedback loop with the NVU to the regulating astroctyes. Further, we identified potentially antagonistic signaling roles for opioid receptor species that should be further investigated for potential therapeutic targets.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12148062 | PMC |
| http://dx.doi.org/10.1101/2025.03.03.640886 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Stabilizing the retromer complex rescues synaptic dysfunction and endosomal trafficking deficits in an Alzheimer's disease mouse model.
Acta Neuropathol Commun
September 2025
Department of Biomedical and Clinical Sciences and Department of Clinical Pathology, Linköping University, 58185, Linköping, Sweden.
Disruptions in synaptic transmission and plasticity are early hallmarks of Alzheimer's disease (AD). Endosomal trafficking, mediated by the retromer complex, is essential for intracellular protein sorting, including the regulation of amyloid precursor protein (APP) processing. The VPS35 subunit, a key cargo-recognition component of the retromer, has been implicated in neurodegenerative diseases, with mutations such as L625P linked to early-onset AD.
View Article and Find Full Text PDFExploring Differentially Expressed Genes and Understanding the Underlying Mechanisms in Glioblastoma.
Biochem Genet
September 2025
Department of Medical Biology, Cerrahpasa Faculty of Medicine, Istanbul University Cerrahpasa, Kocamustafapasa, 34098, Istanbul, Turkey.
Glioblastoma is the most aggressive and malignant tumor of the central nervous system. Current treatment options, including surgical excision, radiotherapy, and chemotherapy, have Limited efficacy, with a median survival rate of approximately 15 months. To develop novel therapeutics, it is crucial to understand the underlying molecular mechanisms driving glioblastoma.
View Article and Find Full Text PDFPotential molecular mechanisms explaining progressive alterations of the structural network in temporal lobe epilepsy.
Neurobiol Dis
September 2025
Department of Neurology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China. Electronic address:
The effect of recurrent seizures on the gradual deterioration of the white matter structural network and the potential molecular mechanisms that underlie the baseline and longitudinal changes in network topology in temporal lobe epilepsy (TLE) remain unclear. Therefore, we used diffusion tensor imaging (DTI) scans and neuropsychiatric assessments for 28 patients with unilateral TLE at baseline and follow-up, and for 28 healthy controls (HC). The topological properties of the structural network were calculated using graph theoretical analyses.
View Article and Find Full Text PDFLoss of hepatic ME1 ameliorates MASLD by Suppressing peroxisomal β-Oxidation and Activating Lipophagy/Lipolysis.
J Adv Res
September 2025
School of Public Health and Nursing, Zhejiang Key Laboratory of Medical Epigenetics, Hangzhou Normal University, Hangzhou, China. Electronic address:
Introduction: Metabolic dysfunction-associated steatotic liver disease (MASLD) represents an increasing global health problem in association with obesity and insulin resistance without approved pharmacotherapy. Previous studies revealed malic enzyme 1 (ME1) as a susceptibility gene for metabolic disorders in humans. However, the role and mechanisms of ME1 in regulating hepatic lipid metabolism remain largely unclear.
View Article and Find Full Text PDFDecoding NMDAR encephalitis: proteomic markers and computational identification of potential therapeutic pathways.
Brain Behav Immun
September 2025
Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address:
Background: The proteome is a valuable resource for pinpointing therapeutic targets. Therefore, we conducted a proteome-wide Mendelian randomization (MR) study aimed at identifying potential protein markers and therapeutic targets for Anti-N-Methyl-D-Aspartate Receptor Encephalitis (NMDAR-E).
Methods: Protein quantitative trait loci (pQTLs) were obtained from seven published genome-wide association studies (GWASs) focusing on the plasma proteome, resulting in summary-level data for 734 circulating protein markers.