Chemical Modulators of Protein Misfolding and by Pierfausto Seneci

By Pierfausto Seneci

This booklet is a neurochemistry-based better half for Protein Misfolding and Neurodegenerative ailments: Molecular Targets, an Elsevier name via an identical writer publishing in December 2014. whereas the 1st ebook specializes in biology and molecular pursuits, this significant other publication describes how those goals are regulated by way of small molecules and disease-modifying compounds. The booklet starts with a quick advent to how key proteins turn into dysfunctional, and every next bankruptcy describes significant ailment mechanisms in Alzheimer’s and different tauopathies. houses and improvement prestige of those molecular pursuits and ailment mechanisms are completely defined, as are small molecule effectors of autophagy and dis-aggregating brokers.

  • Written to supply accomplished insurance of neurodegenerative disease-modifying compounds
  • Provides discipline-specific chapters that hide medicinal chemistry and medical applications
  • Provides an summary of greater than 2 hundred chemical sessions and lead compounds, performing on chosen molecular goals which are of relevance to any neurodegenerative disorder
  • Coverage of misfolding illnesses, chaperone proteins, ubiquitination and autophagy/oncology makes this ebook compatible for structural neurochemists, chemists, biologists, non-CNS scientists, and scientists drawn to drug discovery

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Extra info for Chemical Modulators of Protein Misfolding and Neurodegenerative Disease

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R. ; Silva, J. R. ; Moliner, V. Computational analysis of human OGA structure in complex with PUGNAc and NAG-thiazoline derivatives. J. Chem. Inf. Model. 2012, 52, 2775–2783. [31] Yuzwa, S. ; Macauley, M. ; Heinonen, J. ; Dennis, R. , et al. A potent mechanism-inspired O-GlcNAcase inhibitor that blocks phosphorylation of tau in vivo. Nat. Chem. Biol. 2008, 4, 483–490. [32] Yuzwa, S. ; Macauley, M. ; Vocadlo, D. J. Increasing O-GlcNAc slows neurodegeneration and stabilizes tau against aggregation.

Safety, tolerability and changes in amyloid b concentrations after administration of a g-secretase inhibitor in volunteers. Clin. Neuropharmacol. 2005, 28, 126–132. [74] Siemers, E. ; Quinn, J. ; Farlow, M. , et al. Effects of a gamma-secretase inhibitor in a randomized study of patients with Alzheimer disease. Neurology 2006, 66, 602–604. [75] Fleisher, A. ; Siemers, E. ; Clark, C. ; Dean, R. , et al. Phase 2 safety trial targeting amyloid beta production with a gamma-secretase inhibitor in Alzheimer disease.

A pleiotropic, moderate activity against a number of tauopathy-relevant targets may be a sensible, although complex therapeutic option. Positive results obtained by treating animals with natural mixtures containing flavonoids indirectly support this theory [127–129]. 41) is a tetrasubstituted imidazole, named after its apoptosis-inducing properties in cells [130]. Its activity is Hsc/Hsp bindingdependent, as proven by affinity chromatography with a supported apoptozole derivative [130]. 3 Hsp70 41 processing of ∆F508-CFTR (cystic fibrosis transmembrane conductance regulator), a mutant, misfolded protein involved in cystic fibrosis [131].

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