Effects of quercetin on the hippocampal proteins of BDNF, CREB, DCX, FOXG1, GDNF, and synapsin II: The potential molecular mechanisms

The available therapeutic ways are not more effective for most diseases owing to their several side adverse effects. Therefore, it is critical to find efficacy and safe alternative compounds. In this case, phytochemical compounds may be employed as supplementary therapeutic materials to reduce the disadvantages of synthetic drugs. Quercetin is the main herbal flavonoid with the potential capacity to increase neuronal survival owing to its unique property to cross the blood-brain barrier (BBB). Neuroprotective activities of this secondary metabolite have been illustrated in several in vitro and in vivo studies, but its molecular function has not been completely understood yet. The potential molecular mechanism of quercetin for survival effect on hippocampal neurogenesis is modulation of brain-derived neurotropic factor (BDNF), cAMP-response element binding protein (CREB), doublecortin (DCX), forkhead box transcription factor G1 (FoxG1), glial cell line-derived neurotrophic factor (GDNF), and synapsin I/synapsin II. Regulation of neurogenesis process via these hippocampal proteins is a promising strategy against neurodegenerative diseases. Therefore, in this mini-review, recent findings about the antineurodegenerative effects of quercetin in both micro- and nanoformulation have been summarized and discussed.

Effects of quercetin on the hippocampal proteins of BDNF, CREB, DCX, FOXG1, GDNF, and synapsin II: The potential molecular mechanisms Keywords:

Hippocampal neurogenesis , Hippocampal proteins , Blood-Brain Barrier , Neurodegenerative Diseases