Peroxiredoxin-6 Released by Astrocytes Contributes to Neuroapoptosis During Ischemia.

Peroxiredoxin-6 (PRDX6), a member of the peroxiredoxin family, has progressively emerged as a possible therapeutic target for a variety of brain diseases, particularly Alzheimer's disease and ischemic stroke. However, the role of PRDX6 in neurons under ischemic conditions has remained elusive. Here, we found that astrocytes could release PRDX6 extracellularly after OGD/R, and that PRDX6 release actually worsened neuroapoptosis under OGD/R. We discovered a unique PRDX6/RAGE/JNK signaling pathway that contributes to the effect of neuroapoptosis. We applied a specific inhibitor of the RAGE signaling pathway in a mouse MCAO model and observed significant alterations in animal behavior. Considered together, our findings show the crucial role of the astrocyte-released PRDX6 in the process of neuroapoptosis caused by OGD/R, and could provide novel insights for investigating the molecular mechanism of protecting brain function from ischemia-reperfusion injury.

Association between myasthenia gravis and cognitive disorders: a PRISMA-compliant meta-analysis.

OBJECTIVE: This meta-analysis assessed the association between myasthenia gravis (MG) and cognitive disorders. METHODS: The PubMed, Web of Science, OVID, EMBASE, CNKI and Wanfang electronic databases were comprehensively searched from inception to October 2020 for relevant studies. The primary outcomes were scores of the cognitive function battery. A random effects model was used to evaluate the cognitive function of patients with MG. RESULTS: Eight cross-sectional studies containing 381 patients and 220 healthy controls were included in this meta-analysis. In relation to global cognitive function, patients with MG performed significantly worse than healthy individuals (SMD = -0.4, 95% CI = -0.63 to -0.16, p < 0.001, I2 = 10%). Specifically, the impaired cognitive domains included language, visuospatial function, information processing, verbal immediate and delayed recall memory, visual immediate recall memory, and response fluency, while attention, executive function, and visual delayed recall memory were unimpaired. The patients with early-onset (SMD= -0.527, 95% CI = -0.855 to -0.199, p = 0.002) and generalized MG (SMD= -0.577, 95% CI = -1.047 to -0.107, p = 0.016) had poorer global cognitive performance than the healthy population. CONCLUSIONS: Patients with MG may have cognitive disorders, including those associated with the domains of language, visuospatial function, information processing, verbal immediate and delayed recall memory, visual immediate recall memory and response fluency. Furthermore, the age of onset and disease severity may be associated with cognitive disorders in patients with MG.

Electroacupuncture protects rats from ischemic brain injury via coffilin in mice.

BACKGROUND: This study aimed to study the expression level of cofilin after electroacupuncture (EA) pretreatment, using ischemic brain injury model in mice. In addition, infarct volume and neurological functions were measured to understand whether electroacupuncture stimulation could restore the functions of the brain. METHODS: Total of 36 mice was randomly divided into three groups: sham group, middle cerebral artery occlusion model (MACO), and middle cerebral artery occlusion model pretreated with EA (MACO + EA). Mice were stimulated at "Baihui (G20)" and "Dazhui (G14)" 24 hours before focal cerebral ischemia. Infarct volume and neuronal function of brain tissue were scored among different experimental groups. The expression level of cofilin and phosphocofilin of brain tissue were evaluated by using Western blot analysis. TUNEL assay was performed to determine the degree of cell apoptosis. RESULTS: Compared with the sham group, the level of cofilin was dramatically reduced in the MACO group. EA pretreatment could reduce the protein level of cofilin, while EA therapy could also upregulate the protein level of phosphocofilin. Improved neuronal function, smaller infarct volume, and reduced neuronal apoptosis were observed among the mice underwent EA before middle artery occlusion. CONCLUSION: Our results from Western blot analysis and TUNEL assay might suggest that the upregulation of cofilin was concerned with the EA protects rats from ischemic brain injury. Cofilin might be a potential target for developing drugs against brain ischemia.