Cudrania cochinchinensis attenuates amyloid β protein-mediated microglial activation and promotes glia-related clearance of amyloid β protein

Wang, Chung Jen; Chen, Chien Chih; Tsay, Huey Jen; Chiang, Feng Yi; Wu, Mine Fong; Shiao, Young‐Ji

doi:10.1186/1423-0127-20-55

Cited by 8 publications

(4 citation statements)

References 32 publications

(43 reference statements)

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“…oAβ and fAβ were prepared as described [ 38 , 39 ]. A diluted solution of Aβs was spotted onto a mica slide and scanned using an Agilent® 5400 atomic force microscope (Molecular Imaging Corporation, Tempe, AZ) as described previously [ 20 , 40 ].…”

Section: Methodsmentioning

confidence: 99%

“…Primary cultures of neonatal cortical microglia were prepared from the cerebral cortex of Sprague Dawley rat pups at postnatal day 5 [ 19 , 20 ]. Briefly, 5-day-old pups were anesthetized with ether and sacrificed by decapitation.…”

Section: Methodsmentioning

confidence: 99%

“…Microglia may respond to minor stimuli, which is a major impediment for the cellular characterization of microglia in vivo [ 18 ]. Isolation of amoeboid microglia from mixed glial cultures is a reliable method to verify the distinct populations of microglial phenotypes in a mixed glial culture [ 19 , 20 ]. In mixed glial culture, the amoeboid cells typically rest on top of the astrocyte monolayer and can appear as proliferating cell clusters promoted by astrocyte-secreted mitogens [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

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Amyloid β peptide-mediated neurotoxicity is attenuated by the proliferating microglia more potently than by the quiescent phenotype

Tsay¹,

Huang

Huang³

et al. 2013

J Biomed Sci

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BackgroundThe 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.ResultsThe present study investigates the phenotypes of isolated microglia on protecting neuron against Aβ-mediated neurotoxicity. Primary microglia were isolated from the mixed glia culture, and were further cultured to distinct phenotypes, designated as proliferating amoeboid microglia (PAM) and differentiated process-bearing microglia (DPM). Their inflammatory phenotypes, response to amyloid β (Aβ), and the beneficial or destructive effects on neurons were investigated. DPM may induce both direct neurotoxicity without exogenous stimulation and indirect neurotoxicity after Aβ activation. On the other hand, PAM attenuates Aβ-mediated neurotoxicity through Aβ phagocytosis and/or Aβ degradation.ConclusionsOur results suggest that the proliferating microglia, but not the differentiated microglia, protect neurons against Aβ-mediated neurotoxicity. This discovery may be helpful on the therapeutic investigation of Alzheimer’s disease.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Amyloid β peptide-mediated neurotoxicity is attenuated by the proliferating microglia more potently than by the quiescent phenotype

Tsay¹,

Huang

Huang³

et al. 2013

J Biomed Sci

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“…Cudrania cochinchinensis attenuated A␤ proteinmediated microglial activation and promoted gliarelated clearance of A␤ protein [199].…”

Section: Natural Productsmentioning

confidence: 96%

Cognitive Enhancers (Nootropics). Part 3: Drugs Interacting with Targets other than Receptors or Enzymes. Disease-Modifying Drugs. Update 2014

Froestl

Pfeifer

Muhs

2014

JAD

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Scientists working in the field of Alzheimer's disease and, in particular, cognitive enhancers, are very productive. The review "Drugs interacting with Targets other than Receptors or Enzymes. Disease-modifying Drugs" was accepted in October 2012. In the last 20 months, new targets for the potential treatment of Alzheimer's disease were identified. Enormous progress was realized in the pharmacological characterization of natural products with cognitive enhancing properties. This review covers the evolution of research in this field through May 2014.

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Pharmacogenomics of Alzheimer’s Disease: Novel Therapeutic Strategies for Drug Development

Cacabelos

Torrellas

et al. 2014

Methods in Molecular Biology

165

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Alzheimer's disease (AD) is a major problem of health and disability, with a relevant economic impact on our society. Despite important advances in pathogenesis, diagnosis, and treatment, its primary causes still remain elusive, accurate biomarkers are not well characterized, and the available pharmacological treatments are not cost-effective. As a complex disorder, AD is a polygenic and multifactorial clinical entity in which hundreds of defective genes distributed across the human genome may contribute to its pathogenesis. Diverse environmental factors, cerebrovascular dysfunction, and epigenetic phenomena, together with structural and functional genomic dysfunctions, lead to amyloid deposition, neurofibrillary tangle formation, and premature neuronal death, the major neuropathological hallmarks of AD. Future perspectives for the global management of AD predict that genomics and proteomics may help in the search for reliable biomarkers. In practical terms, the therapeutic response to conventional drugs (cholinesterase inhibitors, multifactorial strategies) is genotype-specific. Genomic factors potentially involved in AD pharmacogenomics include at least five categories of gene clusters: (1) genes associated with disease pathogenesis; (2) genes associated with the mechanism of action of drugs; (3) genes associated with drug metabolism (phase I and II reactions); (4) genes associated with drug transporters; and (5) pleiotropic genes involved in multifaceted cascades and metabolic reactions. The implementation of pharmacogenomic strategies will contribute to optimize drug development and therapeutics in AD and related disorders.

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Cudrania cochinchinensis attenuates amyloid β protein-mediated microglial activation and promotes glia-related clearance of amyloid β protein

Cited by 8 publications

References 32 publications

Amyloid β peptide-mediated neurotoxicity is attenuated by the proliferating microglia more potently than by the quiescent phenotype

Amyloid β peptide-mediated neurotoxicity is attenuated by the proliferating microglia more potently than by the quiescent phenotype

Cognitive Enhancers (Nootropics). Part 3: Drugs Interacting with Targets other than Receptors or Enzymes. Disease-Modifying Drugs. Update 2014

Pharmacogenomics of Alzheimer’s Disease: Novel Therapeutic Strategies for Drug Development

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