Green oat cognitaven® attenuates mild cognitive impairment by activating the CREB/BDNF/Nrf2/HO-1 pathway and modulating NF-κB/MAPK signaling.

Alzheimer's disease (AD) is a progressive neurodegenerative condition, with mild cognitive impairment (MCI) often presenting as an early symptom. Patients with MCI are more likely to experience subsequent long-term cognitive impairments and memory dysfunction. Currently, there are no effective therapeutic agents available for the clinical treatment of AD due to its highly complex pathogenesis. We investigated the neuroprotective and anti-inflammatory effects of green oat cognitaven® in vitro, using lipopolysaccharide (LPS)-stimulated BV-2 microglial cells, and in vivo, using a scopolamine-injected C57BL/6 J amnesic mouse model. The mice were orally administered green oat cognitaven® (90, 180, and 270 mg/kg/b.w.) for 14 days and injected intraperitoneally with scopolamine (1 mg/kg/b.w.) for 14 days. In vitro, green oat cognitaven® exhibited multiple actions in LPS-stimulated BV-2 microglial cells, including strong inhibition of NO release, significantly reduced inflammatory responses, and anti-inflammatory effects. Green oat cognitaven® also demonstrated vigorous anti-neuroinflammatory activity in these cells, inhibiting the activation and phosphorylation of the NF-κB/MAPK signaling pathway. In vivo, the oral administration of green oat cognitaven® in scopolamine-induced amnesic mice produced significant anti-amnesic effects-preventing spatial learning and memory impairments-and demonstrated potent neuroprotective activity through the upregulation of associated biomarkers, including p-CREB and BDNF protein expression. Further experiments showed that green oat cognitaven® upregulates Nrf2/HO-1 expression and mitigates neuroinflammation by inhibiting NF-κB and MAPK signaling. Overall, our study indicated that green oat cognitaven® is a functional dietary component and explores its therapeutic potential to support the treatment and management of AD-associated MCI.