Current therapeutic approaches for Alzheimer's disease (AD) demonstrate limited efficacy and fail to address disease progression. In the present study, we present HSN-G1, a novel ginsenoside-enriched Show more
Current therapeutic approaches for Alzheimer's disease (AD) demonstrate limited efficacy and fail to address disease progression. In the present study, we present HSN-G1, a novel ginsenoside-enriched pharmaceutical formulation that employs a dual-target mechanism through the modulation of amyloid clearance pathways and cholinergic neurotransmission. HSN-G1 demonstrates a reproducible ginsenoside profile enriched with Re (33.27 mg/g), Rd (25.00 mg/g), and Rg3 stereoisomers (12.18 mg/g), ensuring pharmaceutical-grade reproducibility. HSN-G1 enhanced amyloid-beta (Aβ) clearance in microglial cells, with significantly greater effects observed in SRA-overexpressing cells, suggesting SRA-dependent clearance mechanisms. In APP/PS1 transgenic mice, six-week oral administration of HSN-G1 (100-400 mg/kg) elicited significant dose-dependent improvements in cognitive performance. Male mice exhibited more stable and consistent enhancements in both passive avoidance and spatial memory tests compared to vehicle controls (p < 0.001), while both sexes demonstrated comparable reductions in brain Aβ levels (approximately 45%) and differential increases in acetylcholine (73% in males; 55% in females, p < 0.01). HSN-G1 administration enhanced the expression of neurotrophic factors, with NGF upregulation predominantly observed in males, whereas BDNF, CNTF, and GDNF were consistently elevated across both sexes. These findings establish HSN-G1 as a promising disease-modifying agent with standardized composition and therapeutic efficacy, surpassing the limitations of conventional single-target approaches. The superior efficacy of HSN-G1 compared to existing treatments validates its potential for clinical development, highlighting the significance of sex-specific therapeutic responses in future AD therapeutics. Show less
MicroRNAs, as key regulators in gene expression, may hold the key to understanding Alzheimer disease (AD) pathogenesis and diagnosis. To explore the expression level of miR-106b-3p in the serum of AD Show more
MicroRNAs, as key regulators in gene expression, may hold the key to understanding Alzheimer disease (AD) pathogenesis and diagnosis. To explore the expression level of miR-106b-3p in the serum of AD patients, and evaluate its diagnostic value for AD. A total of 250 AD patients and 200 healthy controls were enrolled. Real-time quantitative PCR with fluorescence detection was used to determine the relative expression level of miR-106b-3p. Correlation was analyzed by the Pearson linear correlation analysis. The receiver operating characteristic was used to evaluate the diagnostic efficacy of serum miR-106b-3p for AD. In vitro AD cellular models were established to explore the potential mechanism of miR-106b-3p in AD. The expression of miR-106b-3p in the serum of AD patients is significantly elevated, and its level is negatively correlated with the MMSE score. ROC curve analysis shows that it has certain diagnostic value. miR-106b-3p is a risk factor associated with AD. In addition, miR-106b-3p targets BDNF, affects the functions of SH-SY5Y cells, and promotes the occurrence and development of AD. Serum miR-106b-3p is significantly elevated in AD and may serve as a diagnostic biomarker. Preliminary evidence suggests it promotes AD progression by targeting BDNF, highlighting its potential as a therapeutic target for early intervention. Show less