Analysis of glucocorticoid responsive and circadian clock molecules in Alzheimer’s disease brain tissues.

Background Under basal non-stressed brain conditions, a control system that includes an inherent molecular clock activation, immunomodulatory role of glucocorticoids and nuclear factor-kappa B (NF-κB) signaling is essential to prevent excessive inflammation effectively return homeostasis. This results in continuous competition between feedback feedforward control. Chronic stress dysregulated are implicated as significant risk factors for neurodegeneration. In unstimulated mice, the core gene BMAL1 glucocorticoid induced leucine zipper (GILZ, responsive gene) highly expressed hippocampal microglia. The expressions these two genes positively correlated with circulating corticosterone. Mechanistically, GILZ inhibits translocation NF-κB p65 functions anti-inflammatory molecule. on other hand, independent its circadian partner CLOCK, receptor mediated transactivation GILZ. Elevated plasma corticosterone age-related decrease associated increased activation susceptibility neuropathology. We have observed expression hippocampus inversely related IBA1 mouse models Alzheimer’s disease (AD). Taken together, we hypothesize will correlate negatively markers gliosis neurodegenerative diseases. Method evaluated Period (Per1, Per2 Per3); glial cell surface Iba1 GFAP NF-kB inflammatory AD tissues by immunohistochemistry real-time polymerase chain reaction (RT-PCR). Result was reduced pre-frontal cortex tissues, p65, directly Per2. Conclusion could potentially function modulator at intersection three systems.