Age-Related Inflammatory Balance Shift, Nasal Barrier Function, and Cerebro-Morphological Status in Healthy and Diseased Rodents

Increased blood–brain barrier (BBB) permeability and extensive neuronal changes have been described earlier in both healthy pathological aging like apolipoprotein B-100 (APOB-100) amyloid precursor protein (APP)–presenilin-1 (PSEN1) transgenic mouse models. APOB-100 hypertriglyceridemic model is a useful tool to study the link between cerebrovascular pathology neurodegeneration, while APP–PSEN1 humanized of Alzheimer’s disease. The aim current was characterize inflammatory brain with neurodegeneration. Also, cerebro-morphological cognitive alterations investigated. nose-to-brain delivery P-glycoprotein substrate drug (quinidine) monitored disease models compared age-matched controls. Our results revealed an balance shift aged neurodegenerative In normal monocyte chemoattractant protein-1, stem cell factor Rantes were highly upregulated indicating stimulated leukocyte status. mice, vascular endothelial growth (VEGF), platelet-derived (PDGF-BB), interleukin-17A (IL-17A) induced (vascular reaction), mice resistin, IL-17A GM-CSF mostly upregulated. nasal absorption similar blood molecular bypass BBB. learning memory tests showed no difference performance young animals. Based on these results, it can be concluded that various markers chronic inflammation are present diseased cerebro-ventricular dilation also observed. For development proper anti-aging neuroprotective compounds, further studies focusing above targets suggested.