Animals, Genetically Modified

Publication Title: 
Antimicrobial Agents and Chemotherapy

Due to their rapid, potent action on young and mature intraerythrocytic stages, artemisinin derivatives are central to drug combination therapies for Plasmodium falciparum malaria. However, the evidence for emerging parasite resistance/tolerance to artemisinins in southeast Asia is of great concern. A better understanding of artemisinin-related drug activity and resistance mechanisms is urgently needed. A recent transcriptome study of parasites exposed to artesunate led us to identify a series of genes with modified levels of expression in the presence of the drug.

Author(s): 
Deplaine, Guillaume
Lavazec, Catherine
Bischoff, Emmanuel
Natalang, Onguma
Perrot, Sylvie
Guillotte-Blisnick, Micheline
Coppée, Jean-Yves
Pradines, Bruno
Mercereau-Puijalon, Odile
David, Peter H.
Publication Title: 
Acta Pharmacologica Sinica

AIM: To investigate the embryotoxicity of dihydroartemisinin (DHA), the main active metabolite of artemisinin, in zebrafish, and explore the corresponding mechanisms. METHODS: The embryos of wild type and TG (flk1:GFP) transgenic zebrafish were exposed to DHA. Developmental phenotypes of the embryos were observed. Development of blood vessels was directly observed in living embryos of TG (flk1:GFP) transgenic zebrafish under fluorescence microscope.

Author(s): 
Ba, Qian
Duan, Juan
Tian, Jia-qiang
Wang, Zi-liang
Chen, Tao
Li, Xiao-guang
Chen, Pei-zhan
Wu, Song-jie
Xiang, Li
Li, Jing-quan
Chu, Rui-ai
Wang, Hui
Publication Title: 
BMC neuroscience

BACKGROUND: Epidemiological studies have associated estrogen replacement therapy with a lower risk of developing Alzheimer's disease, but a higher risk of developing breast cancer and certain cardiovascular disorders. The neuroprotective effect of estrogen prompted us to determine potential therapeutic impact of soy-derived estrogenic compounds. Transgenic C. elegans, that express human beta amyloid (Abeta), were fed with soy derived isoflavones genistein, daidzein and glycitein (100 microg/ml) and then examined for Abeta-induced paralysis and the levels of reactive oxygen species.

Author(s): 
Gutierrez-Zepeda, Astrid
Santell, Ross
Wu, Zhixin
Brown, Marishka
Wu, Yanjue
Khan, Ikhlas
Link, Christopher D.
Zhao, Baolu
Luo, Yuan
Publication Title: 
The Journal of Neuroscience: The Official Journal of the Society for Neuroscience

Amyloid-beta (Abeta) toxicity has been postulated to initiate synaptic loss and subsequent neuronal degeneration seen in Alzheimer's disease (AD). We previously demonstrated that the standardized Ginkgo biloba extract EGb 761, commonly used to enhance memory and by AD patients for dementia, inhibits Abeta-induced apoptosis in neuroblastoma cells. In this study, we use EGb 761 and its single constituents to associate Abeta species with Abeta-induced pathological behaviors in a model organism, Caenorhabditis elegans.

Author(s): 
Wu, Yanjue
Wu, Zhixin
Butko, Peter
Christen, Yves
Lambert, Mary P.
Klein, William L.
Link, Christopher D.
Luo, Yuan
Publication Title: 
The Journal of Neuroscience: The Official Journal of the Society for Neuroscience

Nerve growth factor (NGF) can induce apoptosis by signaling through the p75 neurotrophin receptor (p75(NTR)) in several nerve cell populations. Cultured embryonic motor neurons expressing p75(NTR) are not vulnerable to NGF unless they are exposed to an exogenous flux of nitric oxide (*NO). In the present study, we show that p75(NTR)-mediated apoptosis in motor neurons involved neutral sphingomyelinase activation, increased mitochondrial superoxide production, and cytochrome c release to the cytosol.

Author(s): 
Pehar, Mariana
Vargas, Marcelo R.
Robinson, Kristine M.
Cassina, Patricia
Díaz-Amarilla, Pablo J.
Hagen, Tory M.
Radi, Rafael
Barbeito, Luis
Beckman, Joseph S.
Publication Title: 
Journal of Neuroscience Research

Amyotrophic lateral sclerosis (ALS) is caused by the progressive degeneration of motor neurons. Mutations in the Cu/Zn superoxide dismutase (SOD1) are found in approximately 20% of patients with familial ALS. Mutant SOD1 causes motor neuron death through an acquired toxic property. Although the molecular mechanism underlying this toxic gain-of-function remains unknown, evidence support the role of mutant SOD1 expression in nonneuronal cells in shaping motor neuron degeneration.

Author(s): 
Vargas, Marcelo R.
Pehar, Mariana
Díaz-Amarilla, Pablo J.
Beckman, Joseph S.
Barbeito, Luis
Publication Title: 
Neurobiology of Aging

Heat shock response, mediated by heat shock proteins, is a highly conserved physiological process in multicellular organisms for reestablishment of cellular homeostasis. Expression of heat shock factors and subsequent heat shock protein plays a role in protection against proteotoxicity in invertebrate and vertebrate models. Proteotoxicity due to beta-amyloid peptide (Abeta) oligomerization has been linked to the pathogenesis of Alzheimer's disease.

Author(s): 
Wu, Yanjue
Cao, Zhiming
Klein, William L.
Luo, Yuan
Publication Title: 
BMC neuroscience

BACKGROUND: Dysfunctions in the serotonergic system have been implicated in several neurological disorders such as depression. Elderly individuals who have been diagnosed with clinical depression show elevated cases of neurodegenerative diseases. This has led to suggestions that modulating the serotonin (5-HT) system could provide an alternative method to current therapies for alleviating these pathologies. The neuroprotective effects of bilobalide in vitro have been documented. We aim to determine whether bilobalide affects the 5-HT system in the nematode C. elegans.

Author(s): 
Brown, Marishka K.
Luo, Yuan
Publication Title: 
PloS One

BACKGROUND: Proving the efficacy and corresponding mode of action of herbal supplements is a difficult challenge for evidence-based herbal therapy. A major hurdle is the complexity of herbal preparations, many of which combine multiple herbs, particularly when the combination is assumed to be vitally important to the effectiveness of the herbal therapy. This issue may be addressed through the use of contemporary methodology and validated animal models.

Author(s): 
Yu, Young-Beob
Dosanjh, Laura
Lao, Lixing
Tan, Ming
Shim, Bum Sang
Luo, Yuan
Publication Title: 
Neuropharmacology

Alzheimer's disease (AD) is a progressive neurodegenerative disorder and is the most common form of dementia in elderly people. The accumulation of amyloid beta (Abeta) is one of the histopathological hallmarks of AD. Abeta is aggregated to form oligomers which are toxic to neurons and are critical to the onset and progression of AD. In a Caenorhabditis elegans (C. elegans) model of AD, human Abeta is expressed intracellularly in the body wall muscle. The expression and subsequent aggregation of Abeta in the muscle lead to progressive paralysis.

Author(s): 
Keowkase, Roongpetch
Aboukhatwa, Marwa
Luo, Yuan

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