Paula Agostinho

Summary

Affiliation: University of Coimbra
Country: Portugal

Publications

  1. ncbi request reprint Cdk5 acts as a mediator of neuronal cell cycle re-entry triggered by amyloid-beta and prion peptides
    Joao P Lopes
    Center for Neuroscience and Cell Biology, Faculty of Medicine, Biochemistry Institute, University of Coimbra, Coimbra, Portugal
    Cell Cycle 8:97-104. 2009
  2. ncbi request reprint Neuroinflammation, oxidative stress and the pathogenesis of Alzheimer's disease
    Paula Agostinho
    Center for Neurosciences of Coimbra, Faculty of Medicine Pólo I 1st floor, Rua Larga, University of Coimbra, 3004 504 Coimbra, Portugal
    Curr Pharm Des 16:2766-78. 2010
  3. doi request reprint Overactivation of calcineurin induced by amyloid-beta and prion proteins
    Paula Agostinho
    Institute of Biochemistry, Faculty of Medicine, University of Coimbra, 3004 504 Coimbra, Portugal
    Neurochem Int 52:1226-33. 2008
  4. pmc Antagonistic interaction between adenosine A2A receptors and Na+/K+-ATPase-α2 controlling glutamate uptake in astrocytes
    Marco Matos
    Department of Neurology, Boston University School of Medicine, Boston, Massachusetts 02118, CNC Center for Neuroscience and Cell Biology, University of Coimbra, 3004 517 Coimbra, Portugal, and FMUC Faculty of Medicine, University of Coimbra, 3004 504 Coimbra, Portugal
    J Neurosci 33:18492-502. 2013
  5. doi request reprint Galantamine protects against oxidative stress induced by amyloid-beta peptide in cortical neurons
    Joana B Melo
    Center for Neurosciences and Cell Biology, Faculty of Medicine, University of Coimbra, Coimbra, Portugal
    Eur J Neurosci 29:455-64. 2009
  6. doi request reprint Neurodegeneration in an Abeta-induced model of Alzheimer's disease: the role of Cdk5
    Joao P Lopes
    Center for Neuroscience and Cell Biology, Faculty of Medicine, Biochemistry Institute, University of Coimbra, 3004 Coimbra, Portugal
    Aging Cell 9:64-77. 2010
  7. ncbi request reprint Role of cyclin-dependent kinase 5 in the neurodegenerative process triggered by amyloid-Beta and prion peptides: implications for Alzheimer's disease and prion-related encephalopathies
    Joao P Lopes
    Faculty of Medicine, Center for Neuroscience and Cell Biology, Biochemistry Institute, University of Coimbra, 3004, Coimbra, Portugal
    Cell Mol Neurobiol 27:943-57. 2007
  8. ncbi request reprint Prion protein aggregation and neurotoxicity in cortical neurons
    Joana Barbosa Melo
    Center for Neurosciences and Cell Biology, Faculty of Medicine, University of Coimbra, Rua Larga, 3004 504 Coimbra, Portugal
    Ann N Y Acad Sci 1096:220-9. 2007
  9. doi request reprint Astrocytic adenosine A2A receptors control the amyloid-β peptide-induced decrease of glutamate uptake
    Marco Matos
    CNC Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal
    J Alzheimers Dis 31:555-67. 2012
  10. ncbi request reprint Comparative study of microglia activation induced by amyloid-beta and prion peptides: role in neurodegeneration
    Pedro Garção
    Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal
    J Neurosci Res 84:182-93. 2006

Collaborators

Detail Information

Publications22

  1. ncbi request reprint Cdk5 acts as a mediator of neuronal cell cycle re-entry triggered by amyloid-beta and prion peptides
    Joao P Lopes
    Center for Neuroscience and Cell Biology, Faculty of Medicine, Biochemistry Institute, University of Coimbra, Coimbra, Portugal
    Cell Cycle 8:97-104. 2009
    ..Therefore, cell cycle reactivation mediated by Cdk5 can underlie the neurodegenerative processes that occur in AD and PRE...
  2. ncbi request reprint Neuroinflammation, oxidative stress and the pathogenesis of Alzheimer's disease
    Paula Agostinho
    Center for Neurosciences of Coimbra, Faculty of Medicine Pólo I 1st floor, Rua Larga, University of Coimbra, 3004 504 Coimbra, Portugal
    Curr Pharm Des 16:2766-78. 2010
    ..Thus, therapeutic strategies directed at controlling the activation of microglia and astrocytes and the excessive production of pro-inflammatory and pro-oxidant factors may be valuable to control neurodegeneration in dementia...
  3. doi request reprint Overactivation of calcineurin induced by amyloid-beta and prion proteins
    Paula Agostinho
    Institute of Biochemistry, Faculty of Medicine, University of Coimbra, 3004 504 Coimbra, Portugal
    Neurochem Int 52:1226-33. 2008
    ..Therefore, therapeutic strategies targeting CaN might be valuable for these neurodegenerative disorders...
  4. pmc Antagonistic interaction between adenosine A2A receptors and Na+/K+-ATPase-α2 controlling glutamate uptake in astrocytes
    Marco Matos
    Department of Neurology, Boston University School of Medicine, Boston, Massachusetts 02118, CNC Center for Neuroscience and Cell Biology, University of Coimbra, 3004 517 Coimbra, Portugal, and FMUC Faculty of Medicine, University of Coimbra, 3004 504 Coimbra, Portugal
    J Neurosci 33:18492-502. 2013
    ....
  5. doi request reprint Galantamine protects against oxidative stress induced by amyloid-beta peptide in cortical neurons
    Joana B Melo
    Center for Neurosciences and Cell Biology, Faculty of Medicine, University of Coimbra, Coimbra, Portugal
    Eur J Neurosci 29:455-64. 2009
    ..Overall, these results constitute the first evidence that galantamine can prevent the neuronal oxidative damage induced by Abeta, providing an in vitro basis for the beneficial actions of galantamine in the AD neurodegenerative process...
  6. doi request reprint Neurodegeneration in an Abeta-induced model of Alzheimer's disease: the role of Cdk5
    Joao P Lopes
    Center for Neuroscience and Cell Biology, Faculty of Medicine, Biochemistry Institute, University of Coimbra, 3004 Coimbra, Portugal
    Aging Cell 9:64-77. 2010
    ....
  7. ncbi request reprint Role of cyclin-dependent kinase 5 in the neurodegenerative process triggered by amyloid-Beta and prion peptides: implications for Alzheimer's disease and prion-related encephalopathies
    Joao P Lopes
    Faculty of Medicine, Center for Neuroscience and Cell Biology, Biochemistry Institute, University of Coimbra, 3004, Coimbra, Portugal
    Cell Mol Neurobiol 27:943-57. 2007
    ..This study demonstrates, for the first time, that Cdk5 is involved in PrP-neurotoxicity. Altogether, our data suggests that Cdk5 plays an active role in the pathogenesis of AD and PRE...
  8. ncbi request reprint Prion protein aggregation and neurotoxicity in cortical neurons
    Joana Barbosa Melo
    Center for Neurosciences and Cell Biology, Faculty of Medicine, University of Coimbra, Rua Larga, 3004 504 Coimbra, Portugal
    Ann N Y Acad Sci 1096:220-9. 2007
    ....
  9. doi request reprint Astrocytic adenosine A2A receptors control the amyloid-β peptide-induced decrease of glutamate uptake
    Marco Matos
    CNC Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal
    J Alzheimers Dis 31:555-67. 2012
    ..These results provide the first demonstration for a direct key role of astrocytic A(2A)R in the ability of Aβ-induced impairment of glutamate uptake, which may underlie glutamatergic synaptic dysfunction and excitotoxicity in AD...
  10. ncbi request reprint Comparative study of microglia activation induced by amyloid-beta and prion peptides: role in neurodegeneration
    Pedro Garção
    Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal
    J Neurosci Res 84:182-93. 2006
    ..Taken together, the data indicate that Abeta and PrP peptides caused microglia activation and differentially affected cytokine secretion. The IL-6 released by reactive microglia caused neuronal injury...
  11. ncbi request reprint Amyloid beta-peptide 25-35 reduces [3H]acetylcholine release in retinal neurons. Involvement of metabolic dysfunction
    Joana Barbosa Melo
    Center for Neurosciences of Coimbra, Faculty of Medicine, University of Coimbra, 3004 504 Coimbra, Portugal
    Amyloid 9:221-8. 2002
    ....
  12. doi request reprint Activation of cell cycle proteins in transgenic mice in response to neuronal loss but not amyloid-beta and tau pathology
    Joao P Lopes
    Center for Neuroscience and Cell Biology, Faculty of Medicine, Biochemistry Institute, University of Coimbra, Coimbra, Portugal
    J Alzheimers Dis 16:541-9. 2009
    ..Taken together, our data indicate that neuronal cell cycle reactivation is not a prominent feature induced by Abeta or tau pathology, but rather appears to be triggered by acute neuronal loss...
  13. pmc Blockade of adenosine A2A receptors prevents interleukin-1β-induced exacerbation of neuronal toxicity through a p38 mitogen-activated protein kinase pathway
    Ana Patrícia Simões
    Center for Neurosciences of Coimbra, Institute of Biochemistry, Faculty of Medicine, University of Coimbra, 3004 504 Coimbra, Portugal
    J Neuroinflammation 9:204. 2012
    ..We investigated whether A(2A)R controls the signaling of IL-1β and its deleterious effects in cultured hippocampal neurons...
  14. ncbi request reprint Subsynaptic localization of nicotinic acetylcholine receptor subunits: A comparative study in the mouse and rat striatum
    Pedro Garção
    CNC Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal FMUC Faculty of Medicine, University of Coimbra, Coimbra, Portugal
    Neurosci Lett 566:106-10. 2014
    ....
  15. ncbi request reprint Involvement of oxidative stress in the enhancement of acetylcholinesterase activity induced by amyloid beta-peptide
    Joana Barbosa Melo
    Center for Neurosciences of Coimbra and Faculty of Medicine, University of Coimbra, 3004 504 Coimbra, Portugal
    Neurosci Res 45:117-27. 2003
    ....
  16. ncbi request reprint Synaptic and sub-synaptic localization of amyloid-β protein precursor in the rat hippocampus
    Diana I Rodrigues
    CNC Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal
    J Alzheimers Dis 40:981-92. 2014
    ....
  17. doi request reprint Adenosine A2A receptors modulate glutamate uptake in cultured astrocytes and gliosomes
    Marco Matos
    Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal
    Glia 60:702-16. 2012
    ....
  18. doi request reprint Cdk5: multitasking between physiological and pathological conditions
    Joao P Lopes
    Center for Neuroscience and Cell Biology, Faculty of Medicine, Biochemistry Institute, University of Coimbra, 3004 Coimbra, Portugal
    Prog Neurobiol 94:49-63. 2011
    ....
  19. pmc Presynaptic CB(1) cannabinoid receptors control frontocortical serotonin and glutamate release--species differences
    Samira G Ferreira
    Center for Neuroscience and Cell Biology of Coimbra, Faculty of Medicine, University of Coimbra, 3004 517 Coimbra, Portugal
    Neurochem Int 61:219-26. 2012
    ..Altogether, this is the first study to demonstrate functional presynaptic CB(1)Rs in frontocortical glutamatergic and serotonergic terminals, revealing species differences...
  20. ncbi request reprint Involvement of calcineurin in the neurotoxic effects induced by amyloid-beta and prion peptides
    Paula Agostinho
    Center for Neurosciences and Faculty of Medicine, University of Coimbra, 3004 504 Coimbra Portugal
    Eur J Neurosci 17:1189-96. 2003
    ..Taken together these data suggest that calcineurin is involved in A beta 25-35 and PrP106-126 neurotoxicity...
  21. ncbi request reprint Expression and subcellular localization of a novel nuclear acetylcholinesterase protein
    Susana Constantino Rosa Santos
    Instituto de Biopatologia Química, Faculdade de Medicina de Lisboa, 1649 028 Lisboa, Portugal
    J Biol Chem 282:25597-603. 2007
    ..Overall, our studies suggest that the 55-kDa AChE may be involved in different biological processes such as neural development, tumor progression, and angiogenesis...
  22. ncbi request reprint [Neuroprotection strategies: effect of vinpocetine in vitro oxidative stress models]
    Claudia Pereira
    Departamento de Zoologia e Centro de Neurociencias, Faculdade de Medicina, Universidade de Coimbra, Coimbra
    Acta Med Port 16:401-6. 2003
    ....