Trans-cinnamaldehyde Improves Neuroinflammation-mediated NMDA Receptor Dysfunction and Memory Deficits through Blocking NF-κB Pathway in Presenilin1/2 Conditional Double Knockout Mice

Publication date: Available online 31 July 2019Source: Brain, Behavior, and ImmunityAuthor(s): Yang Zhao, Haiyan Deng, Kun Li, Lijun Wang, Yongkang Wu, Xianwen Dong, Xingyu Wang, Yongjun Chen, Ying XuAbstractA chronic neuroinflammatory response has been considered as a critical pathogenesis promoting neurodegenerative progression in Alzheimer’s disease (AD). During neuroinflammatory process, microglia are excessively activated and simultaneously release numerous pro-inflammatory mediators that cause synaptic dysfunction in the forebrain prior to neuronal degeneration and memory deficits in AD. Thus, prevention of neuroinflammation-mediated synaptic dysfunction may be a potential therapeutic approach against neurodegenerative disorders. Trans-cinnamaldehyde (TCA) is a primary bioactive component derived from the stem bark of Cinnamomum cassia, and it possesses potent anti-inflammatory and neuroprotective activities in in vivo and in vitro experiments. However, the in-depth molecular mechanisms of TCA underlying anti-neuroinflammatory and neuroprotective effects on memory deficits in AD are still unclear. The presenilin 1 and 2 conditional double knockout (PS cDKO) mice exhibit AD-like phenotypes including obvious neuroinflammatory responses and synaptic dysfunction and memory deficits. Here, PS cDKO were used to evaluate the potential neuroprotective effects of TCA against neuroinflammation-mediated dementia by performing behavioral tests, electrophysiological recordings and...
Source: Brain, Behavior, and Immunity - Category: Neurology Source Type: research