Fernanda G De Felice

Summary

Affiliation: Rio de Janeiro
Country: Brazil

Publications

  1. ncbi Inflammation, defective insulin signaling, and mitochondrial dysfunction as common molecular denominators connecting type 2 diabetes to Alzheimer disease
    Fernanda G De Felice
    Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
    Diabetes 63:2262-72. 2014
  2. pmc Amyloid-β triggers the release of neuronal hexokinase 1 from mitochondria
    Leonardo M Saraiva
    Programa de Bioquimica e Biofisica Celular, Instituto de Bioquimica Medica, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil
    PLoS ONE 5:e15230. 2010
  3. doi How does brain insulin resistance develop in Alzheimer's disease?
    Fernanda G De Felice
    Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil Electronic address
    Alzheimers Dement 10:S26-32. 2014
  4. pmc Alzheimer's disease and insulin resistance: translating basic science into clinical applications
    Fernanda G De Felice
    Institute of Medical Biochemistry, CCS, Room H2 019, Federal University of Rio de Janeiro, Rio de Janeiro, RJ 21944 590, Brazil
    J Clin Invest 123:531-9. 2013
  5. ncbi Beta-amyloid production, aggregation, and clearance as targets for therapy in Alzheimer's disease
    Fernanda G De Felice
    Departamento de Bioquimica Medica, Instituto de Ciencias Biomedicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil
    Cell Mol Neurobiol 22:545-63. 2002
  6. ncbi Cyclic AMP enhancers and Abeta oligomerization blockers as potential therapeutic agents in Alzheimer's disease
    Fernanda G De Felice
    Instituto de Bioquimica Medica, Programa de Bioquimica e Biofisica Celular, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ 21944 590, Brazil
    Curr Alzheimer Res 4:263-71. 2007
  7. ncbi Targeting the neurotoxic species in Alzheimer's disease: inhibitors of Abeta oligomerization
    Fernanda G De Felice
    Departamento de Bioquimica Medica, Instituto de Ciencias Biomedicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ 21944 590, Brazil
    FASEB J 18:1366-72. 2004
  8. pmc Protection of synapses against Alzheimer's-linked toxins: insulin signaling prevents the pathogenic binding of Abeta oligomers
    Fernanda G De Felice
    Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208, USA
    Proc Natl Acad Sci U S A 106:1971-6. 2009
  9. ncbi Novel neuroprotective, neuritogenic and anti-amyloidogenic properties of 2,4-dinitrophenol: the gentle face of Janus
    Fernanda G De Felice
    Instituto de Bioquimica Medica, Programa de Bioquimica e Biofisica Celular, Universidade Federal do Rio de Janeiro, Brazil
    IUBMB Life 58:185-91. 2006
  10. ncbi Soluble oligomers from a non-disease related protein mimic Abeta-induced tau hyperphosphorylation and neurodegeneration
    Marcelo N N Vieira
    Programa de Bioquimica e Biofisica Celular, Instituto de Bioquimica Medica, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil
    J Neurochem 103:736-48. 2007

Collaborators

Detail Information

Publications30

  1. ncbi Inflammation, defective insulin signaling, and mitochondrial dysfunction as common molecular denominators connecting type 2 diabetes to Alzheimer disease
    Fernanda G De Felice
    Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
    Diabetes 63:2262-72. 2014
    ..Identification of central and peripheral inflammation as potential mediators of brain dysfunction in AD may lead to the development of effective treatments for this devastating disease. ..
  2. pmc Amyloid-β triggers the release of neuronal hexokinase 1 from mitochondria
    Leonardo M Saraiva
    Programa de Bioquimica e Biofisica Celular, Instituto de Bioquimica Medica, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil
    PLoS ONE 5:e15230. 2010
    ..2-deoxyglucose blocked Aβ-induced oxidative stress and neuronal death. Results suggest that Aβ-induced cellular redistribution and inactivation of neuronal HKI play important roles in oxidative stress and neurodegeneration in AD...
  3. doi How does brain insulin resistance develop in Alzheimer's disease?
    Fernanda G De Felice
    Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil Electronic address
    Alzheimers Dement 10:S26-32. 2014
    ..Discoveries summarized here provide pathophysiological background for identification of novel molecular targets and for development of alternative therapeutic approaches in AD...
  4. pmc Alzheimer's disease and insulin resistance: translating basic science into clinical applications
    Fernanda G De Felice
    Institute of Medical Biochemistry, CCS, Room H2 019, Federal University of Rio de Janeiro, Rio de Janeiro, RJ 21944 590, Brazil
    J Clin Invest 123:531-9. 2013
    ..Furthermore, I discuss a rational basis for the use of antidiabetic agents as novel and potentially effective therapeutics in AD...
  5. ncbi Beta-amyloid production, aggregation, and clearance as targets for therapy in Alzheimer's disease
    Fernanda G De Felice
    Departamento de Bioquimica Medica, Instituto de Ciencias Biomedicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil
    Cell Mol Neurobiol 22:545-63. 2002
    ..3. Significant progress has been achieved in these directions, opening up new perspectives toward the development of effective approaches for the treatment or prevention of AD...
  6. ncbi Cyclic AMP enhancers and Abeta oligomerization blockers as potential therapeutic agents in Alzheimer's disease
    Fernanda G De Felice
    Instituto de Bioquimica Medica, Programa de Bioquimica e Biofisica Celular, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ 21944 590, Brazil
    Curr Alzheimer Res 4:263-71. 2007
    ..Possible implications of these findings in the development of novel therapeutic approaches in AD are discussed...
  7. ncbi Targeting the neurotoxic species in Alzheimer's disease: inhibitors of Abeta oligomerization
    Fernanda G De Felice
    Departamento de Bioquimica Medica, Instituto de Ciencias Biomedicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ 21944 590, Brazil
    FASEB J 18:1366-72. 2004
    ..These findings provide a basis for the development of novel small molecule Abeta inhibitors with potential applications in AD...
  8. pmc Protection of synapses against Alzheimer's-linked toxins: insulin signaling prevents the pathogenic binding of Abeta oligomers
    Fernanda G De Felice
    Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208, USA
    Proc Natl Acad Sci U S A 106:1971-6. 2009
    ..The finding that synapse vulnerability to ADDLs can be mitigated by insulin suggests that bolstering brain insulin signaling, which can decline with aging and diabetes, could have significant potential to slow or deter AD pathogenesis...
  9. ncbi Novel neuroprotective, neuritogenic and anti-amyloidogenic properties of 2,4-dinitrophenol: the gentle face of Janus
    Fernanda G De Felice
    Instituto de Bioquimica Medica, Programa de Bioquimica e Biofisica Celular, Universidade Federal do Rio de Janeiro, Brazil
    IUBMB Life 58:185-91. 2006
    ....
  10. ncbi Soluble oligomers from a non-disease related protein mimic Abeta-induced tau hyperphosphorylation and neurodegeneration
    Marcelo N N Vieira
    Programa de Bioquimica e Biofisica Celular, Instituto de Bioquimica Medica, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil
    J Neurochem 103:736-48. 2007
    ....
  11. ncbi Neuritogenesis and neuronal differentiation promoted by 2,4-dinitrophenol, a novel anti-amyloidogenic compound
    Ana Paula Wasilewska-Sampaio
    Instituto de Bioquimica Medica, Programa de Bioquimica e Biofisica Celular, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ Brazil
    FASEB J 19:1627-36. 2005
    ....
  12. ncbi Small molecule inhibitors of lysozyme amyloid aggregation
    Marcelo N N Vieira
    Instituto de Bioquimica Medica, Programa de Bioquimica e Biofisica Celular, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil
    Cell Biochem Biophys 44:549-53. 2006
    ..These results suggest that these small molecule compounds may serve as prototypes for the development of drugs for the prevention or treatment of different types of amyloidoses...
  13. ncbi TNF-α mediates PKR-dependent memory impairment and brain IRS-1 inhibition induced by Alzheimer's β-amyloid oligomers in mice and monkeys
    Mychael V Lourenco
    Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, Rio de Janeiro, RJ 21941 902, Brazil
    Cell Metab 18:831-43. 2013
    ..Results reveal pathogenic mechanisms shared by AD and diabetes and establish that proinflammatory signaling mediates oligomer-induced IRS-1 inhibition and PKR-dependent synapse and memory loss...
  14. ncbi Monoclonal antibodies that target pathological assemblies of Abeta
    Mary P Lambert
    Department of Neurobiology and Physiology, Northwestern University, Evanston, Illinois 60208, USA
    J Neurochem 100:23-35. 2007
    ....
  15. pmc An anti-diabetes agent protects the mouse brain from defective insulin signaling caused by Alzheimer's disease- associated Aβ oligomers
    Theresa R Bomfim
    Institute of Medical Biochemistry, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
    J Clin Invest 122:1339-53. 2012
    ..By establishing molecular links between the dysregulated insulin signaling in AD and diabetes, our results open avenues for the investigation of new therapeutics in AD...
  16. ncbi Abeta oligomers induce neuronal oxidative stress through an N-methyl-D-aspartate receptor-dependent mechanism that is blocked by the Alzheimer drug memantine
    Fernanda G De Felice
    Department of Neurobiology and Physiology, Northwestern University, Evanston, Illinois 60208, USA
    J Biol Chem 282:11590-601. 2007
    ....
  17. pmc Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers
    Fernanda G De Felice
    Department of Neurobiology and Physiology, Northwestern University, 2205 Tech Drive, Evanston, IL 60208, USA
    Neurobiol Aging 29:1334-47. 2008
    ..A beta oligomers have been increasingly implicated as the main neurotoxins in AD, and the current results provide a unifying mechanism in which oligomer activity is directly linked to tau hyperphosphorylation in AD pathology...
  18. doi N-methyl-D-aspartate receptors are required for synaptic targeting of Alzheimer's toxic amyloid-β peptide oligomers
    Helena Decker
    Institute of Medical Biochemistry, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
    J Neurochem 115:1520-9. 2010
    ..Establishing that NMDARs are key components of the synaptic oligomer binding complex may illuminate the development of novel approaches to prevent synapse failure triggered by Aβ oligomers...
  19. pmc Amyloid-β oligomers induce differential gene expression in adult human brain slices
    Adriano Sebollela
    Institute of Medical Biochemistry, Federal University of Rio de Janeiro, Rio de Janeiro, RJ 21944 590, Brazil
    J Biol Chem 287:7436-45. 2012
    ..The results provide insight into early mechanisms of pathogenesis of AD and suggest that the neuronal pathways affected by AβOs may be targets for the development of novel diagnostic or therapeutic approaches...
  20. ncbi Soluble protein oligomers as emerging toxins in Alzheimer's and other amyloid diseases
    Sergio T Ferreira
    Instituto de Bioquimica Medica, Universidade Federal do Rio de Janeiro, Riode Janeiro, RJ 21944 590, Brazil
    IUBMB Life 59:332-45. 2007
    ..Increased understanding of the cellular toxic mechanisms triggered by protein oligomers may lead to the development of rational, effective treatments for amyloid disorders...
  21. ncbi Amyloid beta oligomers induce impairment of neuronal insulin receptors
    Wei Qin Zhao
    Department of Neurobiology and Physiology, Northwestern University, 2205 Tech Dr, Hogan 5 110, Evanston, IL 60280, USA
    FASEB J 22:246-60. 2008
    ....
  22. pmc Activation of D1/D5 dopamine receptors protects neurons from synapse dysfunction induced by amyloid-beta oligomers
    Sofia Jürgensen
    Institute of Medical Biochemistry, Federal University of Rio de Janeiro, Rio de Janeiro RJ 1944 590, Brazil
    J Biol Chem 286:3270-6. 2011
    ..Results suggest that D1/D5 receptors may be relevant targets for development of novel pharmacological approaches to prevent synapse failure in AD...
  23. ncbi Expression profile of rat hippocampal neurons treated with the neuroprotective compound 2,4-dinitrophenol: up-regulation of cAMP signaling genes
    Adriano Sebollela
    Instituto de Bioquimica Medica, Programa de Bioquimica e Biofisica Celular, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21944 590, Brazil
    Neurotox Res 18:112-23. 2010
    ..Results shed light on molecular mechanisms underlying neuroprotection by DNP and point to possible targets for development of novel therapeutics for neurodegenerative disorders...
  24. ncbi Metastable, partially folded states in the productive folding and in the misfolding and amyloid aggregation of proteins
    Sergio T Ferreira
    Instituto de Bioquimica Medica, Programa de Bioquimica e Biofisica Celular, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil
    Cell Biochem Biophys 44:539-48. 2006
    ..Here, we review recent examples of the use of hydrostatic pressure as a tool to gain insight into the forces and energetics governing the productive folding or the misfolding and amyloid aggregation of proteins...
  25. doi Memantine rescues transient cognitive impairment caused by high-molecular-weight aβ oligomers but not the persistent impairment induced by low-molecular-weight oligomers
    Claudia P Figueiredo
    School of Pharmacy, Federal University of Rio de Janeiro, Rio de Janeiro, RJ 21944 590, Brazil
    J Neurosci 33:9626-34. 2013
    ..Furthermore, results suggest a mechanistic explanation for the limited efficacy of memantine in preventing memory loss in AD...
  26. ncbi Activation of GABA(A) receptors by taurine and muscimol blocks the neurotoxicity of beta-amyloid in rat hippocampal and cortical neurons
    Andrea C Paula-Lima
    Instituto de Bioquimica Medica, Programa de Bioquimica e Biofisica Celular, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ 21941 590, Brazil
    Neuropharmacology 49:1140-8. 2005
    ....
  27. ncbi Formation of soluble oligomers and amyloid fibrils with physical properties of the scrapie isoform of the prion protein from the C-terminal domain of recombinant murine prion protein mPrP-(121-231)
    Samantha M Martins
    Programa de Bioquimica e Biofisica Celular, Instituto de Bioquimica Medica, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ 21944 590, Brazil
    J Biol Chem 281:26121-8. 2006
    ....
  28. ncbi Mitochondrial bound hexokinase activity as a preventive antioxidant defense: steady-state ADP formation as a regulatory mechanism of membrane potential and reactive oxygen species generation in mitochondria
    Wagner Seixas da-Silva
    Departamento de Bioquimica Medica, Universidade Federal do Rio de Janeiro, Cidade Universitaria, Rio de Janeiro, Rio de Janeiro 21941 590, Brazil
    J Biol Chem 279:39846-55. 2004
    ....
  29. doi Inflammation, defective insulin signaling, and neuronal dysfunction in Alzheimer's disease
    Sergio T Ferreira
    Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil Electronic address
    Alzheimers Dement 10:S76-83. 2014
    ..We also explore the contribution of brain inflammation to defective insulin signaling and neuronal dysfunction. Last, we review recent evidence indicating that targeting neuroinflammation may provide novel therapeutic avenues for AD...
  30. ncbi Formation of amyloid aggregates from human lysozyme and its disease-associated variants using hydrostatic pressure
    Fernanda G De Felice
    Departamento de Bioquimica Medica, Instituto de Ciencias Biomedicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ 21944 590, Brazil
    FASEB J 18:1099-101. 2004
    ....