Avenanthramide-C Mitigates High-Fat Diet-Accelerated Alzheimer's Pathologies via NOD1-Driven Neuroinflammation in 5×FAD Mice.

: Obesity is clinically known to be associated with an increased risk and aggravated pathology of Alzheimer's disease (AD). A high-fat diet (HFD), the major contributor to obesity, induces neuroinflammation and central insulin resistance, both of which are linked to synaptic dysfunction. Our previous studies demonstrated that avenanthramide-C (Avn-C), a natural oat-derived phenolic compound, exerts anti-inflammatory effects and alleviates synaptic dysfunction in conventional AD models.

Acute Restraint Stress Induces Long-Lasting Synaptic Enhancement by Inhibiting AMPK Activation in AD Model Mice.

Background: Alzheimer's disease (AD) is characterized by a gradual synaptic loss. The progression of AD severely affects late-phase long-term potentiation (L-LTP), which is essential for long-term memory consolidation.

Aim: We have previously demonstrated the beneficial effects of acute restraint stress (ARS) on hippocampal LTP in AD mouse models.

Avenanthramide C Prevents Neuronal Apoptosis via PI3K/Akt/GSK3β Signaling Pathway Following Middle Cerebral Artery Occlusion.

Avenanthramides are a group of phenolic alkaloids that have been shown to have anti-inflammatory, anti-oxidant, anti-atherogenic, and vasodilation effects. The aim of the present study was to investigate the neuroprotective effect of avenanthramide-c (Avn-c) in focal brain ischemia and reperfusion injury using middle cerebral artery occlusion (MCAo) model with mice. Male C57BL/6 mice were divided into 4 groups: sham, control (MCAo), Avn-c, and Avn-c + LY294002 (phosphoinositide 3-kinase inhibitor) group.