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| First Name: | Valentina | | Last Name: | Echeverria | | Title: | Biochemist | | Advanced Degrees: | PhD | | Affiliation: | Bay pines VA Health care system | | Department: | Research & development | | Street Address 1: | 10,000 Bay Pines | | Street Address 2: | Bldg22, Rm123 | | City: | Bay Pines | | State/Province: | FL | | Zip/Postal Code: | 33744 | Country/Territory: | U.S.A. | | Email Address: |  |
Disclosure:
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Member reports no financial or other potential conflicts of interest. [Last Modified: 3 January 2008]
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View all comments by Valentina Echeverria
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Alzheimer Disease, Tauopathies, Aging Process, Parkinson Disease, Stroke and Trauma
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Tau/Cytoskeleton, Molecular and Cell biology, Neurobiology, Signal transduction, Neuropathology, Animal Models, Oxidative Stress, A-beta PP/A-beta
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University, Research institute
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1. Echeverria V, Clerman A., Doré, S. Stimulation of PGE receptors EP2 and EP4 protects cultured neurons against oxidative stress and cell death following beta-amyloid exposure. Eur J Neurosc.22(9): 2199-206, 2005
2. Echeverria V, Ducatenzeiler A, Chen CH, Cuello AC. Endogenous beta- amyloid peptide synthesismodulates cAMP response element-regulated gene expression in PC12 cells. Neuroscience. 135(4): 1193-202, 2005
3.Echeverria V, Ducatenzeiler A, Dowd E, Janne J, Grant SM, Szyf M, Wandosell F, Avila J, Grimm H, Dunnett SB, Hartmann T, Alhonen L, Cuello AC. Altered mitogen-activated protein kinase signaling, tau hyperphosphorylation and mild spatial learning dysfunction in transgenic rats expressing the beta-amyloid peptide intracellularly in hippocampal and cortical neurons. Neuroscience. 129(3):583-92, 2004
4. Echeverria V, Ducatenzeiler A, Alhonen L, Janne J, Grant SM, Wandosell F, Muro A, Baralle F, Li H, Duff K, Szyf M, Cuello AC. Rat transgenic models with a phenotype of intracellular Abeta accumulation in hippocampus and cortex.J Alzheimers Dis.6(3):209-19, 2004
5. Echeverria V, Cuello AC. Intracellular A-beta amyloid, a sign for worse things to come? Mol Neurobiol.26(2-3):299-316. Review, 2002
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The physiological function of Amyloid b-peptide
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Amyloid b-peptide at physiological levels participates promoting neuronal plasticity
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