Astragalus membranaceus is commonly used in traditional Chinese medicine for strengthening the host defense system. Astragalus membranaceus-polysaccharides is an effective component with various important bioactivities, such as immunomodulation, antioxidant, anti-diabetes, anti-inflammation and neuroprotection. In the present study, we determine the effects of Astragalus membranaceus-polysaccharides on metabolically stressed transgenic mice in order to develop this macromolecules for treatment of sporadic Alzheimer’s disease, a neurodegenerative disease with metabolic risk factors. Transgenic mice, at 10 weeks old prior to the appearance of senile plaques, were treated in combination of administrating high-fat diet and injecting low-dose streptozotocin to create the metabolically stressed mice model. Astragalus membranaceus-polysaccharides was administrated starting at 14 weeks for 7 weeks. We found that Astragalus membranaceus-polysaccharides reduced metabolic stress-induced increase of body weight, insulin and insulin and leptin level, insulin resistance, and hepatic triglyceride. Astragalus membranaceus-polysaccharides also ameliorated metabolic stress-exacerbated oral glucose intolerance, although the fasting blood glucose was only temporally reduced. In brain, metabolic stress-elicited astrogliosis and microglia activation in the vicinity of plaques was also diminished by Astragalus membranaceus-polysaccharides administration. The plaque deposition, however, was not significantly affected by Astragalus membranaceus-polysaccharides administration. These findings suggest that Astragalus membranaceus-polysaccharides may be used to ameliorate metabolic stress-induced diabesity and the subsequent neuroinflammation, which improved the behavior performance in metabolically stressed transgenic mice.

The specific role of microglia on Aβ-mediated neurotoxicity is difficult to assign in vivo due to their complicated environment in the brain. Therefore, most of the current microglia-related studies employed the isolated microglia. However, the previous in vitro studies have suggested either beneficial or destructive function in microglia. Therefore, to investigate the phenotypes of the isolated microglia which exert activity of neuroprotective or destructive is required.

The accumulation of soluble oligomeric amyloid-β peptide (oAβ) proceeding the formation of senile plaques contributes to synaptic and memory deficits in Alzheimer’s disease. Our previous studies have indentified scavenger receptor A (SR-A), especially SR-A type I (SR-AI), as prominent scavenger receptors on mediating oAβ clearance by microglia while glycan moiety and scavenger receptor cysteine-rich (SRCR) domain may play the critical role. Macrophage receptor with collagenous structure (MARCO), another member of class A superfamily with a highly conserved SRCR domain, may also play the similar role on oAβ internalization. However, the role of N-glycosylation and SRCR domain of SR-AI and MARCO on oAβ internalization remains unclear. We found that oAβ internalization was diminished in the cells expressing SR-AI harboring mutations of dual N-glycosylation sites (i.e. N120Q-N143Q and N143Q-N184Q) while they were normally surface targeted. Normal oAβ internalization was observed in 10 SR-AI-SRCR and 4 MARCO-SRCR surface targeted mutants. Alternatively, the SRCR mutants at β-sheet and α-helix and on disulfide bone formation obstructed receptor’s N-glycosylation and surface targeting. Our study reveals that N-glycan moiety is more critical than SRCR domain for SR-A-mediated oAβ internalization.

Subacute low back pain (sLBP) is a critical transitional phase between acute and chronic stages and is key in determining the progression to chronic pain. While persistent pain has been linked to changes in brain activity, studies have focused mainly on acute and chronic phases, leaving neural changes during the subacute phase—especially during movement—under-researched. This cross-sectional study aimed to investigate changes in brain activity and the impact of pain intensity in individuals with sLBP during rest and reaching movements. Using a 28-electrode EEG, we measured motor-related brain waves, including theta, alpha, beta, and gamma oscillations. Transitioning from rest to movement phases resulted in significant reductions (> 80%) in mean power across all frequency bands, indicating dynamic brain activation in response to movement. Furthermore, pain intensity was significantly correlated with brain wave activity. During rest, pain intensity was positively correlated with alpha oscillation activity in the central brain area (r = 0.40, p < 0.05). In contrast, during movement, pain intensity was negatively correlated with changes in brain activity (r = -0.36 to -0.40, p < 0.05). These findings suggest that pain influences brain activity differently during rest and movement, underscoring the impact of pain levels on neural networks related to the sensorimotor system in sLBP and highlighting the importance of understanding neural changes during this critical transitional phase.