Modified TPP-MoS2 QD Blend as a Bio-Functional Model for Normalizing Microglial Dysfunction in Alzheimer’s Disease

Alzheimer’s disease (AD) is the most prevalent neurodegenerative of old age. Accumulation β-amyloid peptide (Aβ) and mitochondrial dysfunction results in chronic microglial activation, which enhances neuroinflammation promotes neurodegeneration. Microglia are resident macrophages brain spinal cord play an important role maintaining homeostasis through a variety phenotypes, including pro-inflammatory phenotype anti-inflammatory phenotypes. However, persistently activated cells generate reactive species neurotoxic mediators. Therefore, inhibitors activation seen to have promise AD control. The modified TPP/MoS2 QD blend mitochondrion-targeted nanomaterial that exhibits cytoprotective activities antioxidant properties scavenging free radicals. In present study, cell viability cytotoxicity DSPE-PEG-TPP/MoS2 on stimulated by Aβ were investigated. levels oxygen (ROS) membrane potential (MMP) also assessed. addition, cytokines, such as tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), transforming growth beta (TGF-β), inducible nitric oxide synthase (iNOS) arginase-1 (Arg-I) measured presence or absence immortalized microglia accumulation Aβ. We found was biocompatible nontoxic at specific concentrations. Furthermore, significantly reduced release radicals improved function upregulation MMP dose-dependent manner treated with pre-treatment concentrations 25 50 μg/mL prior stimulation inhibited expression IL-1β, IL-6, TNF-α, iNOS. Nevertheless, cytokines TGF-β Arg-I activated. These findings suggest oxidative stress, inflammation (IMG) Overall, our research shows has therapeutic for managing can impact polarization.