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Invasive plant species pose significant ecological and economic threats due to their establishment and dominance in non-native ranges. Previous studies have yielded mixed results regarding the plants' adaptive mechanisms for thriving in new environments, and particularly, little is known about how the phenotypic plasticity of growth and defense-related traits may facilitate plant invasion. This study addressed these uncertainties by employing the aggressive weed Reynoutria japonica as a study model. We examined the differences in growth, defense-related traits and biomass allocation between R. japonica populations from native and introduced ranges grown in two common gardens with distinct climate conditions. Our results demonstrated that while the introduced populations did not exhibit increases in height and total dry mass, nor reductions in leaf defense levels, their investment in leaf production was significantly higher compared to the native populations. Additionally, introduced populations displayed greater phenotypic plasticity in clonal ramet but less phenotypic plasticity in biomass production than native populations across varying environments. These findings highlight the roles of phenotypic plasticity and specific trait adaptations, such as clonality, in the successful invasion of R. japonica. This study has important implications for managing invasive plant species under changing environmental conditions. [ABSTRACT FROM AUTHOR]

Abstract Curcumin,a natural polyphenol obtained from turmeric,has been implicated to be neuroprotective in a variety of neurodegenerative disorders although the mechanism remains poorly understood. The results of our recent experiments indicated that curcumin could protect dopaminergic neurons from apoptosis in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson’s disease (PD). The death of dopaminergic neurons and the loss of dopaminergic axon in the striatum were significantly suppressed by curcumin in MPTP mouse model. Further studies showed that curcumin inhibited JNKs hyperphosphorylation induced by MPTP treatment. JNKs phosphorylation can cause translocation of Bax to mitochondria and the release of cytochrome c which both ultimately contribute to mitochondria-mediated apoptosis. These pro-apoptosis effect can be diminished by curcumin. Our experiments demonstrated that curcumin can prevent nigrostriatal degeneration by inhibiting the dysfunction of mitochondrial through suppressing hyperphosphorylation of JNKs induced by MPTP. Our results suggested that JNKs/mitochondria pathway may be a novel target in the treatment of PD patients.

Abstract Background Increasing evidence suggests that microglial activation may participate in the aetiology and pathogenesis of Parkinson's disease (PD). CD200-CD200R signalling has been shown to be critical for restraining microglial activation. We have previously shown that expression of CD200R in monocyte-derived macrophages, induced by various stimuli, is impaired in PD patients, implying an intrinsic abnormality of CD200-CD200R signalling in PD brain. Thus, further in vivo evidence is needed to elucidate the role of malfunction of CD200-CD200R signalling in the pathogenesis of PD. Methods 6-hydroxydopamine (6-OHDA)-lesioned rats were used as an animal model of PD. CD200R-blocking antibody (BAb) was injected into striatum to block the engagement of CD200 and CD200R. The animals were divided into three groups, which were treated with 6-OHDA/Veh (PBS), 6-OHDA/CAb (isotype control antibody) or 6-OHDA/BAb, respectively. Rotational tests and immunohistochemistry were employed to evaluate motor deficits and dopaminergic neurodegeneration in animals from each group. HPLC analysis was used to measure monoamine levels in striatum. Morphological analysis and quantification of CD11b- (or MHC II-) immunoreactive cells were performed to investigate microglial activation and possible neuroinflammation in the substantia nigra (SN). Finally, ELISA was employed to assay protein levels of proinflammatory cytokines. Results Compared with 6-OHDA/CAb or 6-OHDA/Veh groups, rats treated with 6-OHDA/BAb showed a significant increase in counts of contralateral rotation and a significant decrease in TH-immunoreactive (TH-ir) neurons in SN. A marked decrease in monoamine levels was also detected in 6-OHDA/BAb-treated rats, in comparison to 6-OHDA/Veh-treated ones. Furthermore, remarkably increased activation of microglia as well as up-regulation of proinflammatory cytokines was found concomitant with dopaminergic neurodegeneration in 6-OHDA/BAb-treated rats. Conclusions This study shows that deficits in the CD200-CD200R system exacerbate microglial activation and dopaminergic neurodegeneration in a 6-OHDA-induced rat model of PD. Our results suggest that dysfunction of CD200-CD200R signalling may be involved in the aetiopathogenesis of PD.

Abstract Microglia cells are the brain counterpart of macrophages and function as the first defense in the brain. Although they are neuroprotective in the young brain, microglia cells may be primed to react abnormally to stimuli in the aged brain and to become neurotoxic and destructive during neurodegeneration. Aging-induced immune senescence occurs in the brain as age-associated microglia senescence, which renders microglia to function abnormally and may eventually promote neurodegeneration. Microglia senescence is manifested by both morphological changes and alterations in immunophenotypic expression and inflammatory profile. These changes are likely caused by microinvironmental factors, but intrinsic factors cannot yet be completely excluded. Microglia senescence appears to underlie the switching of microglia from neuroprotective in the young brain to neurotoxic in the aged brain. The hypothesis of microglia senescence during aging offers a novel perspective on their roles in aging-related neurodegeneration. In Parkinson's disease and Alzheimer's disease, over-activation of microglia may play an active role in the pathogenesis because microglia senescence primes them to be neurotoxic during the development of the diseases.

Alzheimer's disease (AD) is one of most common neurodegenerative diseases, which gradually begins and develops after 65 years old, presenting as progressive and irreversible memory loss and other cognitive decline, and finally causes dementia and disability. Therefore, early diagnosis, timely treatment and effective prevention of AD have been become important clinical and scientific problems. During the period of Twelfth Five-Year Plan for National Economic and Social Development, our team have engaged in AD diagnosis and treatment for a long time and carried out studies in the field of pathogenesis, epidemiology, screening of risk factors, neuropsychological tests, imaging, biomarkers and early intervention of AD. This paper has summarized these research achievements. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) is one of the most common neurodegenerative diseases. Because of its high prevalence, severe disability and chronic course of disease, it has become one of the most important research focuses in modern medicine ranging from early diagnosis and treatment to prevention. During the period of Twelfth Five-Year Plan for National Economic and Social Development, our team made use of previously established PD Clinical Databse and applying basic research platform, focused on clinical and basic development of PD, and further extended our investigation into the field of pathogenesis, diagnosis and treatment in PD with characteristics of translational medicine. Several progresses have been made in a multiple of aspects: 1) a novel cellular mechanism of mitochondrial fission with the involvement of VPS35 gene, dysregulation of which might be involved in the pathogenesis of familial and sporadic PD. 2) The predictive value of autonomic dysfunction and dopamine transporter (DAT) PET in identifying patients with idiopathic rapid eye movement sleep behavior disorder (iRBD) with a high risk of progressing into neurodegenerative synucleinopathy diseases could form a basis for future disease - prevention trials. Additionally, we initiated the research on PD mortality rate and analyzed the common reasons of death, which added to the evidence of clinical prognosis and progression. 3) We issued the first, second and third versions of "Chinese guidelines for treatment of Parkinson's disease", as well as the "Diagnostic criteria of Parkinson's disease in China (2016 edition)", which could help improve the diagnostic ability and optimize the clinical treatment of PD in China. [ABSTRACT FROM AUTHOR]

Abstract: Cerebral amyloid angiopathy is a common feature in Alzheimer’s disease (AD), which is characterized by amyloid deposit around brain vessels including capillaries. The origin of the amyloid protein of CAA remains controversial. In our work, we provide data to show that primary umbilical vein endothelial cells (HUVEC) harbor APP processing secretases and can produce Aβ42 under starvation. Starvation can increase the secretion of Aβ42 by altering the expression of β-secretases (BACE1) and γ-secretases (APH and PEN2). This process is regulated by macroautophagy. Suppression of macroautophagy induction by 3MA further increased the level of Aβ42 produced under starvation in HUVECs. These results suggest that starvation-induced Aβ42 secretion might contribute to the formation of CAA and hence vascular degeneration in AD. [Copyright &y& Elsevier]

In the title mol-ecule, C(23)H(21)NO, the dihedral angle between the planes of the indole ring and naphthalene ring system is 68.8 (5)°.

Alzheimer's disease (AD) is the most common age-related neurodegenerative disorder. Accumulating data indicate that astrocytes play an important role in the neuroinflammation related to the pathogenesis of AD. It has been shown that microglia and astrocytes are activated in AD brain and amyloid-beta (Abeta) can increase the expression of cyclooxygenase 2 (COX-2), interleukin-1, and interleukin-6. Suppressing the inflammatory response caused by activated astrocytes may help to inhibit the development of AD. Curcumin is a major constituent of the yellow curry spice turmeric and proved to be a potential anti-inflammatory drug in arthritis and colitis. There is a low age-adjusted prevalence of AD in India, a country where turmeric powder is commonly used as a culinary compound. Curcumin has been shown to suppress activated astroglia in amyloid-beta protein precursor transgenic mice. The real mechanism by which curcumin inhibits activated astroglia is poorly understood. Here we report that the expression of COX-2 and glial fibrillary acidic protein were enhanced and that of peroxisome proliferator-activated receptor gamma (PPARgamma) was decreased in Abeta(25-35)-treated astrocytes. In line with these results, nuclear factor-kappaB translocation was increased in the presence of Abeta. All these can be reversed by the pretreatment of curcumin. Furthermore, GW9662, a PPARgamma antagonist, can abolish the anti-inflammatory effect of curcumin. These results show that curcumin might act as a PPARgamma agonist to inhibit the inflammation in Abeta-treated astrocytes.