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| First Name: | Carlos A. | | Last Name: | Saura | | Title: | Research Assistant Professor | | Advanced Degrees: | PhD | | Affiliation: | Universitat Autonoma Barcelona | | Department: | Institut of Neuroscience | | Street Address 1: | Edifici M, M2-118 | | City: | Bellaterra (Cerdanyola Valles) | | State/Province: | Barcelona | | Zip/Postal Code: | 08193 | Country/Territory: | Spain | | Phone: | 34-935814827 | | Fax: | 34 935814152 | | Email Address: |  |
Disclosure:
(view policy)
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Member reports no financial or other potential conflicts of interest. [Last Modified: 24 May 2004]
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View all comments by Carlos A. Saura
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A-beta PP/A-beta, Animal Models, Neuropathology, Neurobiology, Signal transduction
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1988-1993 B.S. University of Barcelona, Spain (Chemistry)
1993-1995 Master University of Barcelona, Spain (Biochemistry)
1995-1998 Ph.D University of Barcelona, Spain (Chemistry)
Postdoctoral Training and Current Position:
1998-1999 Postdoctoral Fellow, Department of Pathology, Johns Hopkins University
1999-2000 Postdoctoral Fellow, Department Neurobiology, Pharmacology & Physiology, University of Chicago
2000-2002 Research Fellow, Department of Neurology,
Harvard Medical School
2002- 2004 Instructor in Neurology, Department of Neurology, Harvard Medical School
2004- Research Assistant Professor, Institut of Neuroscience, Universitat Autonoma Barcelona, Spain |
1.Saura, C. A.et al. Loss of Presenilin function causes impairments of memory and synaptic plasticity followed by age-dependent neurodegeneration. Neuron 42 (1):23-36 (2004)
2.Gines,S., Ivanova,E., Seong,I-S, Saura,C.A and MacDonald, M. .E. Enhanced Akt signaling is an early pro-survival response that reflects N-Methyl-D-aspartate receptor activation in Huntington’s disease knock-in striatal cells. J.Biol. Chem. 278(50):50514-50522 (2003)
3. Yu, H.* et al. APP processing and synaptic plasticity in Presenilin-1 conditional knockout mice. Neuron, 2001; 31 (5): 713-726.
4. Leem, J.Y.et al A role of presenilin 1 in regulating the delivery of amyloid precursor protein to the cell surface. Neurobiol. Dis., 2002; 11 (1): 64-82.
5. Saura, C.A. et al. The non-conserved hydrophilic loop domain of presenilin (PS) is not required for PS endoproteolysis or enhanced Ab42 production mediated by familial early-onset Alzheimer’s disease-linked PS variants. J. Biol. Chem. 2000; 275 (22): 17136-17142
6.Saura, C.A., et al Evidence that intramolecular associations between Presenilin domains are obligatory for endoproteolytic processing. J. Biol. Chem. 1999; 274 (20): 13818-13823.
7. Saura, C. A. et al Adenosine deaminase and A1 adenosine receptors internalize together following agonist-induced receptor desensitization. J. Biol. Chem. 1998; 273 (28): 17610-17617.
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Early causes of memory dysfunction in AD |
PNAS 2004; 101: 7141-7146
PNAS 2004; 101:8162-8167
Ann Neurol 2004; 55:617-626 |
Therapy using AD animal models |
Synaptic and memory impairments are early events in AD. Presenilin dysfunction cause FAD by Ab-dependent and independet mechanisms. |
Early synaptic dysfunction is an early event in AD.
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