Highly Localized Surface Plasmon Nanolasers via Strong Coupling.

Surface plasmons have robust and strong confinement to the light field which is beneficial for the light-matter interaction. Surface plasmon amplification by stimulated emission of radiation (SPACER) has the potential to be integrated on the semiconductor chip as a compact coherent light source, which can play an important role in further extension of Moore's law. In this study, we demonstrate the localized surface plasmon lasing at room temperature in the communication band using metallic nanoholes as the plasmonic nanocavity and InP nanowires as the gain medium. Optimizing laser performance has been demonstrated by coupling between two metallic nanoholes which adds another degree of freedom for manipulating the lasing properties. Our plasmonic nanolasers exhibit lower power consumption, smaller mode volumes, and higher spontaneous emission coupling factors due to enhanced light-matter interactions, which are very promising in the applications of high-density sensing and photonic integrated circuits.

Molecular Characterization and Epidemiology of Carbapenem-Resistant Enterobacteriaceae Isolated from Pediatric Patients in Guangzhou, Southern China.

Background: Carbapenem-resistant Enterobacteriaceae (CRE) are spreading worldwide, posing a serious public health concern. However, the data on CRE strains that cause infections in children in Guangzhou remain limited. Therefore, this study aimed to investigate the epidemiology of CRE, drug resistance, and resistance mechanisms in children in Guangzhou, Southern China. Methods: In total, 54 nonrepetitive CRE strains were collected in pediatric patients at three centers in Guangzhou, Southern China, from January 2016 to August 2018. CRE isolates were used for further studies on antimicrobial susceptibility, the modified Hodge test (MHT), the modified carbapenem inactivation method (mCIM), and drug resistance genes. Multilocus sequence typing (MLST) was used to elucidate the molecular epidemiology of K. pneumoniae. Results: The isolated CRE strains include 34 K. pneumoniae (63.0%), 10 E. coli (18.5%), 4 Enterobacter cloacae (7.4%), and 6 Proteus mirabilis (11.1%) strains. The strains were isolated mainly from the blood (31.5%, n = 17), sputum (31.5%, n = 17), and urine (16.7%, n = 9). All CRE isolates were highly resistant to the third- or fourth-generation cephalosporins, carbapenems, and ß-lactam + ß-lactamase inhibitors (94.4%-96.3%). In addition, the resistance rates to amikacin, ciprofloxacin, levofloxacin, tigecycline, and colistin were 5.6%, 14.8%, 16.7%, 9.3%, and 0%, respectively. Carbapenemase was detected in 35 (64.8%) of the CRE isolates. The most dominant carbapenemase gene was bla NDM (n = 17, 48.6%), followed by bla IMP (n = 13, 37.1%) and bla OXA-23 (n = 4, 11.4%). Other carbapenemase genes (bla KPC, bla sim, bla Aim, bla GES, bla Gim, bla OXA-2 , and bla OXA-48 ) and the mcr-1 gene were not detected. MLST analysis showed high diversity among the K. pneumoniae, and ST45 (11.7%, 4/34) was the dominant sequence type. Conclusion: This study revealed bla NDM was the most dominant carbapenemase gene in children in Guangzhou. Infection control measures need to be taken for the prevention and treatment of CRE infections.

Anti-Cognitive Decline by Yinxing-Mihuan-Oral-Liquid via Activating CREB/BDNF Signaling and Inhibiting Neuroinflammatory Process.

BACKGROUND: Cognitive decline in the normal aging process is one of the most common and prominent problems. Delaying and alleviating cognitive impairment is an important strategy of anti-aging. This study is to aim at investigating the effects of Yinxing-Mihuan-Oral-Liquid(GMOL) on the CREB/BDNF signaling in the normal aging process.METHODS: SD rats were randomly divided into GMOL group and control group. The Morris water maze (MWM) was introduced for behavioral test. Immunohistochemistry and immunofluorescence were used for cAMP response element binding protein 1(CREB1), p-CREB(Ser133), brain-derived neurotrophic factor(BDNF), synaptophysin(SYP) and glial fibrillary acidic protein(GFAP). Western blot was conducted for investigating the levels of CREB1 and p-CREB(Ser133), BDNF, SYP, GFAP and interleukin 6(IL-6). RESULTS:  Our data showed that compared with the control group, GMOL group had higher expression of memory-related proteins, decreased inflammatory factors, and enhanced spatial learning and memory ability.CONCLUSION: The study results show that GMOL ameliorates cognitive impairment of the normal aged SD rats via enhancing the expression of memory biomarkers and inhibiting inflammatory process. The potential neuroprotective role of GMOL in the process of aging may be related to mitigating cognitive decline via activating CREB/BDNF signaling and inhibiting inflammatory process.

Plasmonic Nanolasers Enhanced by Hybrid Graphene-Insulator-Metal Structures.

Graphene is a two-dimensional (2D) structure that creates a linear relationship between energy and momentum that not only forms massless Dirac fermions with extremely high group velocity but also exhibits a broadband transmission from 300 to 2500 nm that can be applied to many optoelectronic applications, such as solar cells, light-emitting devices, touchscreens, ultrafast photodetectors, and lasers. Although the plasmonic resonance of graphene occurs in the terahertz band, graphene can be combined with a noble metal to provide a versatile platform for supporting surface plasmon waves. In this study, we propose a hybrid graphene-insulator-metal (GIM) structure that can modulate the surface plasmon polariton (SPP) dispersion characteristics and thus influence the performance of plasmonic nanolasers. Compared with values obtained when graphene is not used on an Al template, the propagation length of SPP waves can be increased 2-fold, and the threshold of nanolasers is reduced by 50% when graphene is incorporated on the template. The GIM structure can be further applied in the future to realize electrical control or electrical injection of plasmonic devices through graphene.

Ultracompact Pseudowedge Plasmonic Lasers and Laser Arrays.

Concentrating light at the deep subwavelength scale by utilizing plasmonic effects has been reported in various optoelectronic devices with intriguing phenomena and functionality. Plasmonic waveguides with a planar structure exhibit a two-dimensional degree of freedom for the surface plasmon; the degree of freedom can be further reduced by utilizing metallic nanostructures or nanoparticles for surface plasmon resonance. Reduction leads to different lightwave confinement capabilities, which can be utilized to construct plasmonic nanolaser cavities. However, most theoretical and experimental research efforts have focused on planar surface plasmon polariton (SPP) nanolasers. In this study, we combined nanometallic structures intersecting with ZnO nanowires and realized the first laser emission based on pseudowedge SPP waveguides. Relative to current plasmonic nanolasers, the pseudowedge plasmonic lasers reported in our study exhibit extremely small mode volumes, high group indices, high spontaneous emission factors, and high Purell factors beneficial for the strong interaction between light and matter. Furthermore, we demonstrated that compact plasmonic laser arrays can be constructed, which could benefit integrated plasmonic circuits.

No relationship between right-to-left shunt with the severity of white matter hyperintensities.

INTRODUCTION: Studies have shown that right-to-left shunt (RLS) is closely related to the occurrence of white matter hyperintensities (WMHs). Therefore, the detection of RLS is of great significance for the diagnosis and treatment of cerebral small vessel disease, especially for the prevention and treatment of WMHs. In this study, the c-TCD foaming experiment was selected to screen RLS, and evaluate the correlation between RLS and the severity of WMHs. METHODS: We enrolled 334 migraineurs from a multicentre study from July 1 2019 and January 31 2020. Participants were all evaluated using contrast-enhanced transcranial Doppler, magnetic resonance imaging (MRI), and completed a questionnaire covering demographics, the main risk factors of vascular disease, and migraine status. RLS was classified into four grades (Grade 0 = Negative; Grade I = 1 ≤microbubbles (MBs)≤ 10; Grade II = MBs > 10 and no curtain; Grade III = curtain). Silent brain ischemic infarctions (SBI) and white matter hyperintensities (WMHs) were evaluated on MRI. RESULTS: In the incidence of WMHs, we found a significant difference between patients with RLS and no RLS (p < 0.05). There is no relationship between different grades of RLS and the severity of WMHs (p > 0.05). CONCLUSION: Overall, the positive rate of RLS is related to the incidence of WMHs. The different grades of RLS have no-relationship to do with the severity of WMHs.

Prevalence, serotype, and antimicrobial resistance profiles of children infected with Salmonella in Guangzhou, southern China, 2016-2021.

Purpose: Salmonella infection is a key global public health concern and has lead to an increased economic burden on society. We investigated the epidemiological characteristics and antimicrobial resistance profiles of clinically isolated Salmonella strains in Guangzhou Women and Children's Medical Center. Patients and methods: This was a retrospective study of 1,338 Salmonella strains collected from children in Guangzhou Women and Children's Medical Center during 2016 to 2021. Results: The results revealed that 1,338 cases of Salmonella were mainly isolated from feces and blood samples. The age distribution was dominated by infants under 3 years old. The seasonal distribution was high in summer and autumn. 48 serotypes were detected, and S. typhimurium (78.7%) was the predominant serogroup. The results of antimicrobial susceptibility showed that the highest resistance was observed in ampicillin (84.5%), while lower resistance was observed in piperacillin/tazobactam, cefoperazone/sulbactam and ciprofloxacin. The antimicrobial resistance rate of fecal isolates was higher than that of blood isolates. The five-year average detection rate of multi-drug resistant Salmonella was 8.5% (114/1338) and the MDR rate of S. typhimurium was the lowest (6.9%; 73/1053). Conclusion: We concluded that antibacterial treatment should be carefully selected according to serotype and antimicrobial sensitivity results in children. Antimicrobial resistance monitoring for multi-drug resistant Salmonella is still required.

Room-Temperature Gate Voltage Modulation of Plasmonic Nanolasers.

Stable electrical modulation of plasmonic nanolasers is achieved on a hybrid graphene-insulator-metal (GIM) platform at room temperature. To support surface plasmon polariton (SPP) resonance, a zinc oxide (ZnO) nanowire is placed on the GIM platform to create a plasmonic cavity with a compact mode volume of 2.6 × 10-2 λ3, and the graphene layer is used as a transparent electrode for electrical modulation. When a gate voltage is applied, the surface electron density of Al varied, which results in the shifting of its plasma frequency and thus affects its SPP dispersion. In particular, this variation strongly changes the internal loss of the SPP mode; thus, the lasing thresholds of the ZnO nanowire plasmonic nanolasers on the GIM platform can be modulated by the gate voltage. This study demonstrates the gate voltage modulation of ZnO nanowire plasmonic nanolasers on a GIM platform at room temperature. These nanolasers can exhibit ultrahigh modulation speed on the order of terahertz. Accordingly, plasmonic nanolasers with gate voltage modulation have high potential for plasmonic circuit applications with high operation speed and versatility.

Prediction of Prognosis, Immunotherapy and Chemotherapy with an Immune-Related Risk Score Model for Endometrial Cancer.

Endometrial cancer (EC) is the most common gynecologic cancer. The overall survival remains unsatisfying due to the lack of effective treatment screening approaches. Immunotherapy as a promising therapy has been applied for EC treatment, but still fails in many cases. Therefore, there is a strong need to optimize the screening approach for clinical treatment. In this study, we employed co-expression network (GCN) analysis to mine immune-related GCN modules and key genes and further constructed an immune-related risk score model (IRSM). The IRSM was proved effective as an independent predictor of poor prognosis. The roles of IRSM-related genes in EC were confirmed by IHC. The molecular basis, tumor immune microenvironment and clinical characteristics of the IRSM were revealed. Moreover, the IRSM effectiveness was associated with immunotherapy and chemotherapy. Patients in the low-risk group were more sensitive to immunotherapy and chemotherapy than those in the high-risk group. Interestingly, the patients responding to immunotherapy were also more sensitive to chemotherapy. Overall, we developed an IRSM which could be used to predict the prognosis, immunotherapy response and chemotherapy sensitivity of EC patients. Our analysis not only improves the treatment of EC but also offers targets for personalized therapeutic interventions.

Histone H3K79 methylation by DOT1L promotes Aurora B localization at centromeres in mitosis.

Centromere localization of the chromosome passenger complex (CPC) is paramount for achieving accurate sister chromosome segregation in mitosis. Although it has been widely recognized that the recruitment of CPC is directly regulated by two histone codes, phosphorylation of histone H3 at threonine 3 (H3T3ph) and phosphorylation of histone H2A at threonine 120 (H2AT120ph), the regulation of CPC localization by other histone codes remains elusive. We show that dysfunction of disruptor of telomeric silencing 1 like (DOT1L) leads to mislocation of the CPC in prometaphase, caused by disturbing the level of H3T3ph and its reader Survivin. This cascade is initiated by over-dephosphorylation of H3T3ph mediated by the phosphatase RepoMan-PP1, whose scaffold RepoMan translocalizes to chromosomes, while the level of H3K79me2/3 is diminished. Together, our findings uncover a biological function of DOT1L and H3K79 methylation in mitosis and give insight into how genomic stability is coordinated by different histone codes.

Impaired autophagy in amyloid-beta pathology: A traditional review of recent Alzheimer's research.

Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder. The major pathological changes in AD progression are the generation and accumulation of amyloid-beta (Aß) peptides as well as the presence of abnormally hyperphosphorylated tau proteins in the brain. Autophagy is a conserved degradation pathway that eliminates abnormal protein aggregates and damaged organelles. Previous studies have suggested that autophagy plays a key role in the production and clearance of Aß peptides to maintain a steady-state of Aß peptides levels. However, a growing body of evidence suggests that autophagy is significantly impaired in the pathogenesis of AD, especially in Aß metabolism. Therefore, this article reviews the latest studies concerning the mechanisms of autophagy, the metabolism of Aß peptides, and the defective autophagy in the production and clearance of Aß peptides. Here, we also summarize the established and new strategies for targeting autophagy in vivo and through clinical AD trials to identify gaps in our knowledge and to generate further questions.

Diagnostic Value of IGFBP-2 in Predicting Preeclampsia before 20 Weeks of Pregnancy: A Prospective Nested Case-Control Study.

Purpose: To identify novel biomarker insulin-like growth factor binding protein-2 (IGFBP-2) associated with preeclampsia (PE) before 20 weeks of gestation and to explore the predictive value of plasma IGFBP-2 in PE. Methods: A prospective nested case-control investigation involving 122 PE patients and 122 normal controls (NC) that were matched 1 : 1 in terms of age and week of pregnancy was carried out in Guangzhou Women and Children's Medical Center (Guangzhou, China, 2018030306) from April 2016 to December 2019. At 8 to 20 weeks, blood samples from the mother were taken. To calculate the correlations, univariate conditional logistic regression was employed. Results: Herein, 12 clinical indices were significantly different between the PE and NC groups (uric acid (UA), cystatin C (Cys C), aspartate aminotransferase (AST), glutamyl transpeptidase (γ-GT), total bilirubin (TB), prothrombin time (PT), red blood cell (RBC), hematocrit (HCT), red cell distribution width (RDW), platelets (PLT), mean platelet volume (MPV), and thrombocytocrit (PCT)). Compared with the NC group (36.79 ± 19.91 pg/mL), the expression level of IGFBP2 in the PE group (19.76 ± 19.40 pg/mL) before 20 weeks of pregnancy was significantly decreased (P < 0.01). Two high-risk factors were found to be significantly associated with PE independently of confounders: anemia 4.35 (2.20-8.45) (P < 0.01) and cesarean section history 8.25 (2.67-26.67) (P < 0.01). As a result of the univariate logistic regression analysis, the following three variables were included in the final logistic regression model.: Y = -18.841 - 0.085 × (IGFBP-2) + 0.630 × (RDW) + 0.165 × (AST) + 0.863 × (MPV). In comparison to IGFBP-2 alone as an independent predictor of PE (AUC = 0.897, 95% CI 0.830-0.964), the model's discriminatory power was considerably higher (AUC = 0.953, 95% CI 0.911-0.995). Conclusion: Plasma IGFBP-2 before 20 weeks of pregnancy combined with high-risk factors and routine blood indexes has a high early predictive value for PE.

Role of RhoA/ROCK signaling in Alzheimer's disease.

Rho-associated coiled-coil kinase (ROCK), a serine/threonine kinase regulated by the small GTPase RhoA, is involved in regulating cell migration, proliferation, and survival. Numerous studies have shown that the RhoA/ROCK signaling pathway can promote Alzheimer's disease (AD) occurrence. ROCK activation increases ß-secretase activity and promotes amyloid-beta (Aß) production; moreover, Aß further activates ROCK. This is suggestive of a possible positive feedback role for Aß and ROCK. Moreover, ROCK activation promotes the formation of neurofibrillary tangles and abnormal synaptic contraction. Additionally, ROCK activation can promote the neuroinflammatory response by activating microglia and astrocytes to release inflammatory cytokines. Therefore, ROCK is a promising drug target in AD; further, there is a need to elucidate the specific mechanism of action.

Challenges and Advancement of Blue III-Nitride Vertical-Cavity Surface-Emitting Lasers.

Since the first demonstration of (Al, In, Ga)N-based blue vertical-cavity surface-emitting lasers (VCSELs) in 2008, the maximum output power (Pmax) and threshold current density (Jth) has been improved significantly after a decade of technology advancements. This article reviewed the key challenges for the realization of VCSELs with III-nitride materials, such as inherent polarization effects, difficulties in distributed Bragg's reflectors (DBR) fabrication for a resonant cavity, and the anti-guiding effect due to the deposited dielectrics current aperture. The significant tensile strain between AlN and GaN hampered the intuitive cavity design with two epitaxial DBRs from arsenide-based VCSELs. Therefore, many alternative cavity structures and processing technologies were developed; for example, lattice-matched AlInN/GaN DBR, nano-porous DBR, or double dielectric DBRs via various overgrowth or film transfer processing strategies. The anti-guiding effect was overcome by integrating a fully planar or slightly convex DBR as one of the reflectors. Special designs to limit the emission polarization in a circular aperture were also summarized. Growing VCSELs on low-symmetry non-polar and semipolar planes discriminates the optical gain along different crystal orientations. A deliberately designed high-contrast grating could differentiate the reflectivity between the transverse-electric field and transverse-magnetic field, which restricts the lasing mode to be the one with the higher reflectivity. In the future, the III-nitride based VCSEL shall keep advancing in total power, applicable spectral region, and ultra-low threshold pumping density with the novel device structure design and processing technologies.

Bioenergetic Impairment in the Neuro-Glia-Vascular Unit: An Emerging Physiopathology during Aging.

An emerging concept termed the "neuro-glia-vascular unit" (NGVU) has been established in recent years to understand the complicated mechanism of multicellular interactions among vascular cells, glial cells, and neurons. It has been proverbially reported that the NGVU is significantly associated with neurodegenerative disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). Physiological aging is an inevitable progression associated with oxidative damage, bioenergetic alterations, mitochondrial dysfunction, and neuroinflammation, which is partially similar to the pathology of AD. Thus, senescence is regarded as the background for the development of neurodegenerative diseases. With the exacerbation of global aging, senescence is an increasingly serious problem in the medical field. In this review, the coupling of each component, including neurons, glial cells, and vascular cells, in the NGVU is described in detail. Then, various mechanisms of age-dependent impairment in each part of the NGVU are discussed. Moreover, the potential bioenergetic alterations between different cell types in the NGVU are highlighted, which seems to be an emerging physiopathology associated with the aged brain. Bioenergetic intervention in the NGVU may be a new direction for studies on delaying or diminishing aging in the future.

Role of mismatch repair in aging.

A common feature of aging is the accumulation of genetic damage throughout life. DNA damage can lead to genomic instability. Many diseases associated with premature aging are a result of increased accumulation of DNA damage. In order to minimize these damages, organisms have evolved a complex network of DNA repair mechanisms, including mismatch repair (MMR). In this review, we detail the effects of MMR on genomic instability and its role in aging emphasizing on the association between MMR and the other hallmarks of aging, serving to drive or amplify these mechanisms. These hallmarks include telomere attrition, epigenetic alterations, mitochondrial dysfunction, altered nutrient sensing and cell senescence. The close relationship between MMR and these markers may provide prevention and treatment strategies, to reduce the incidence of age-related diseases and promote the healthy aging of human beings.

Ameliorating Ribosylation-Induced Amyloid-ß Pathology by Berberine via Inhibiting mTOR/p70S6K Signaling.

BACKGROUND: Berberine (BBR) plays a neuroprotective role in the pathogenesis of Alzheimer's disease (AD), inhibiting amyloid-ß (Aß) production and promoting Aß clearance. Advanced glycation end products (AGEs) promote Aß aggregation and tau hyperphosphorylation. The activation of mTOR signaling occurring at the early stage of AD has a prominent impact on the Aß production. This work focused on whether BBR regulates the production and clearance of ribosylation-induced Aß pathology via inhibiting mTOR signaling. OBJECTIVE: To explore whether BBR ameliorates ribosylation-induced Aß pathology in APP/PS1 mice. METHODS: Western blot and immunofluorescence staining were used to detect the related proteins of the mammalian target of Rapamycin (mTOR) signaling pathway and autophagy, as well as the related kinases of Aß generation and clearance. Tissue sections and Immunofluorescence staining were used to observe Aß42 in APP/PS1 mice hippocampal. Morris water maze test was used to measure the spatial learning and memory of APP/PS1 mice. RESULTS: BBR improves spatial learning and memory of APP/PS1 mice. BBR limits the activation of mTOR/p70S6K signaling pathway and enhances autophagy process. BBR reduces the activity of BACE1 and γ-secretase induced by D-ribose, and enhances Aß-degrading enzymes and Neprilysin, and inhibits the expression of Aß in APP/PS1 mice. CONCLUSION: BBR ameliorates ribosylation-induced Aß pathology via inhibiting mTOR/p70S6K signaling and improves spatial learning and memory of the APP/PS1 mice.

Role of Hypoxia Inducible Factor-1α in Alzheimer's Disease.

Amyloid-ß (Aß) peptides and hyperphosphorylated tau protein are the most important pathological markers of Alzheimer's disease (AD). Neuroinflammation and oxidative stress are also involved in the development and pathological mechanism of AD. Hypoxia inducible factor-1α (HIF-1α) is a transcriptional factor responsible for cellular and tissue adaption to low oxygen tension. Emerging evidence has revealed HIF-1α as a potential medicinal target for neurodegenerative diseases. On the one hand, HIF-1α increases AßPP processing and Aß generation by promoting ß/γ-secretases and suppressing α-secretases, inactivates microglia and reduces their activity, contributes to microglia death and neuroinflammation, which promotes AD pathogenesis. On the other hand, HIF-1α could resist the toxic effect of Aß, inhibits tau hyperphosphorylation and promotes microglial activation. In summary, this review focuses on the potential complex roles and the future perspectives of HIF-1α in AD, in order to provide references for seeking new drug targets and treatment methods for AD.

Curcumin Prevents Neuroinflammation by Inducing Microglia to Transform into the M2-phenotype via CaMKKß-dependent Activation of the AMP-Activated Protein Kinase Signal Pathway.

BACKGROUND: Neuroinflammation plays an important role in the pathophysiological process of various neurodegenerative diseases. It is well known that curcumin has obvious anti-inflammatory effects in various neuroinflammation models. However, its effect on the modulation of microglial polarization is largely unknown. OBJECTIVE: This study aimed to investigate whether curcumin changed microglia to an anti-inflammatory M2-phenotype by activating the AMP-activated protein kinase (AMPK) signaling pathway. METHODS: LPS treatment was used to establish BV2 cells and primary microglia neuroinflammation models. The neuroinflammation mouse model was established by an intracerebroventricular (ICV) injection of lipopolysaccharide (LPS) in the lateral septal complex region of the brain. TNF-α was measured by ELISA, and cell viability was measured by Cell Counting Kit-8 (CCK-8). The expression of proinflammatory and anti-inflammatory cytokines was examined by Q-PCR and Western blot analysis. Phenotypic polarization of BV2 microglia was detected by immunofluorescence. RESULTS: Curcumin enhanced AMPK activation in BV2 microglial cells in the presence and absence of LPS. Upon LPS stimulation, the addition of curcumin promoted M2 polarization of BV2 cells, as evidenced by suppressed M1 and the elevated M2 signature protein and gene expression. The effects of curcumin were inhibited by an AMPK inhibitor or AMPK knockdown. Calmodulin-dependent protein kinase kinase ß (CaMKKß) and liver kinase B1 (LKB1) are upstream kinases that activate AMPK. Curcumin can activate AMPK in Hela cells, which do not express LKB1. However, both the CaMKKß inhibitor and siRNA blocked curcumin activation of AMPK in LPS-stimulated BV2 cells. Moreover, the CaMKKß inhibitor and siRNA weaken the effect of curcumin suppression on M1 and enhancement of M2 protein and gene expression in LPS-stimulated BV2 cells. Finally, curcumin enhanced AMPK activation in the brain area where microglia were over-activated upon LPS stimulation in an in vivo neuroinflammation model. Moreover, curcumin also suppressed M1 and promoted M2 signature protein and gene expression in this in vivo model. CONCLUSION: Curcumin enhances microglia M2 polarization via the CaMKKß-dependent AMPK signaling pathway. Additionally, curcumin treatment was found to be neuroprotective and thus might be considered as a novel therapeutic agent to treat the neurodegenerative disease such as Alzheimer's disease, Parkinson's disease, etc.

Role of Mitochondrial Dysfunction in the Pathology of Amyloid-ß.

Mitochondrial dysfunction has been widely reported in several neurodegenerative disorders, including in the brains of patients with Alzheimer's disease (AD), Parkinson's disease, and Huntington disease. An increasing number of studies have implicated altered glucose and energy metabolism in patients with AD. There is compelling evidence of abnormalities in some of the key mitochondrial enzymes involved in glucose metabolism, including the pyruvate dehydrogenase and α-ketoglutarate dehydrogenase complexes, which play a great significance role in the pathogenesis of AD. Changes in some of the enzyme activities of the mitochondria found in AD have been linked with the pathology of amyloid-ß (Aß). This review highlights the role of mitochondrial function in the production and clearance of Aß and how the pathology of Aß leads to a decrease in energy metabolism by affecting mitochondrial function.