Activation of the sigma-1 receptor attenuates blood-brain barrier disruption by inhibiting amyloid deposition in Alzheimer's disease mice.

The sigma-1 receptor is an important target for drug development in several neuropsychiatric diseases, including Alzheimer's disease (AD). Accumulating evidence has shown that the integrity and functional activity of the blood-brain barrier (BBB) in AD are impaired, which is closely related to the movement of amyloid beta (Aβ) across the BBB and the formation of Aβ plaques. In this study, we investigated the effects of sigma-1 receptor activation on BBB disruption and Aβ levels in AD mice.

Xanthoceraside attenuates amyloid β peptide-induced memory impairments by reducing neuroinflammatory responses in mice.

Xanthoceraside, a novel triterpenoid saponin extracted from the husks of Xanthoceras sorbifolia Bunge, has neuroprotective effects in vivo and anti-inflammatory properties in vitro. However, the exact mechanism of xanthoceraside on anti-amyloid beta (Aβ)-induced neuroinflammatory responses has not been elucidated. Therefore, we used intracerebroventricular injection of amyloid (Aβ) to establish a mouse model to test the effects of xanthoceraside on Aβ-induced cognitive impairments and the TLR2/NF-κB and MAPK pathways.

Arctigenin Attenuates Learning and Memory Deficits through PI3k/Akt/GSK-3β Pathway Reducing Tau Hyperphosphorylation in Aβ-Induced AD Mice.

Arctigenin is a phenylpropanoid dibenzylbutyrolactone lignan compound possessing antitumor, anti-inflammatory, anti-influenza, antioxidant, antibacterial, and hypoglycaemic activities. Our previous study demonstrated that arctigenin exerts neuroprotective effects both and in a Parkinson's disease model. However, the exact mechanism through which arctigenin improves amyloid beta-induced memory impairment by inhibiting the production of the hyperphosphorylated tau protein is unknown.