(ZGP) treatment for 60 days significantly improved cognitive performance in a transgenic Alzheimer's disease mouse model.
ZGP treatment reduced hippocampal amyloid-β deposition and BACE1 expression.
Suppression of tau phosphorylation was observed at multiple pathological sites (T205, S396, S404).
Restoration of synaptic markers and increased dendritic spine density were noted.
ZGP decreased levels of pro-inflammatory cytokines IL-1β, IL-6, and TNF-α in the hippocampus.
Inhibition of the RAGE/NF-κB signaling pathway was associated with neuroinflammation reduction.
Simplified
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β (Aβ) accumulation, tau hyperphosphorylation, synaptic dysfunction, and chronic neuroinflammation. Current single-target interventions fail to halt disease progression, highlighting the need for multi-target strategies. This study investigates the therapeutic potential and mechanisms of (ZGP), a traditional Chinese medicine formula, in a transgenic AD mouse model. were treated with ZGP for 60 days. Behavioral performance was assessed using the Morris water maze, novel object recognition, and open field test. Aβ deposition, tau phosphorylation, and synaptic integrity were evaluated via immunohistochemistry, Western blotting, RT-qPCR, and Golgi staining. Neuroinflammation and RAGE/NF-κB signaling were analyzed by ELISA and protein expression profiling. Statistical analyses included ANOVA with post hoc Tukey or Bonferroni tests following Shapiro-Wilk and Bartlett's validation. ZGP significantly improved cognitive performance, reduced hippocampal Aβ deposition and BACE1 expression, and suppressed tau phosphorylation at multiple pathological sites (T205, S396, S404). Synaptic markers (Syn, PSD95) were restored, accompanied by increased dendritic spine density. ZGP also reduced hippocampal IL-1β, IL-6, and TNF-α levels and inhibited the RAGE/p-NF-κB pathway. ZGP exerts multi-target neuroprotective effects in 3xTg-AD mice by modulating Aβ and tau pathologies, preserving synaptic structure, and attenuating RAGE-mediated neuroinflammation. These findings support ZGP as a promising integrative therapeutic strategy for AD.
Key numbers
3 of 6
Cognitive Improvement
Proportion of groups showing improved performance in cognitive tests.
2.3×
Reduction in Aβ Levels
Magnitude of decrease in Aβ levels in -treated mice.
3 of 6
Decreased Tau Hyperphosphorylation
Proportion of groups showing reduced p-Tau levels.
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