| |
Nibaldo
C. Inestrosa Ph.D.
Professor, Pontificia Universidad
Católica de Chile; Presidential Chair in Science.
Professor Nibaldo C. Inestrosa, is a world recognized neuroscientist.
Principal investigator of several international and national
research projects, including the Muscular Dystrophy Association
of America and the Flemish Community-Belgium, he was awarded
the Bernardo Houssay Prize of the Argentinian Society of Biology
to the most Productive Young Scientist in Latin America in
the Last Ten Years (1988). Recently, he has been elected as
a member of the Third World Academy of Sciences (TWAS). Professor
Inestrosa has been deeply committed to the formation of graduate
and postgraduate students, serving as advisor to numerous
graduate students. He was twice awarded a Presidential Chair
in Science from the Chilean His research accomplishments are
related to neurotrophic regulation of acetylcholinesterase,
anchorage of AChE to the cell surface, cell biology of amyloid-b-precursor
protein APP and mechanisms of amyloid formation and neurotoxicity.
His current research
aims to understand the mechanism by which the APP, presenilin
and AChE interact intracellularly in order to generate neurotoxic
Ab fibrils. Dr. Inestrosa has been recently appointed Member
of the Chilean Academy of Sciences.
ACADEMIC POSITIONS: Full Professor Pontificia Universidad
Católica de Chile. Visiting Professor for a period of 2 months
in Neuroscience Division, UCSF Department of Pharmacology,
Case Western Res. University, Department of Neurobiology,
Weizmann Inst. of Science.
PUBLICATIONS: 152 original scientific manuscripts with
a total of 845 citations.
SELECTED
PUBLICATIONS
Alvarez, A., Opazo, C., Alarcon, R. and
Inestrosa,
N.C. (1997). Acetylcholinesterase promotes the aggregation
of amyloid-b-peptide fragments by forming a complex with the
growing fibrils. J. Mol. Biol. 272, 348-361.
Alvarez A., Alarcon R., Opazo
C., Campos E.O., Muñoz F.J., Calderon F.H., Dajas F., Gentry
M.K., Doctor B.P., De Mello F.G. and Inestrosa,
N.C. (1998). Stable
complexes involving acetylcholinesterase and amyloid-peptide
change the biochemical properties of the enzyme and increase
the neurotoxicity of Alzheimers fibrils. J. Neurosci. 18, 3213-3223.
Garrido, J.L., Godoy, J., Alvarez,
A., BRONFMAN, M. and INESTROSA, N.C. (2002).
“Protein kinase C inhibits amyloid _-peptide
neurotoxicity by acting on members of the Wnt pathway”. FASEB J. 16: 1982-1984.
INESTROSA, N.C., De Ferrari, G.V., Garrido, J.L., Alvarez,
A., Olivares, G.H., Barría, M.I., BRONFMAN, M. and
Chacón, M.A. (2002). “Wnt signaling involvement in__-amyloid-dependent
neurodegeneration”. Neurochem Int 41: 341-344.
Morgan, C., Bugueño, M.P., Garrido, J. and
INESTROSA, N.C. (2002). “Laminin affects polymerization,
depolymerization and neurotoxicity of A_ peptide”. Peptides 23: 1229-1240.
Muñoz, F.J., Opazo, C., Gil-Gómez,
G., Tapia, G., Fernández, V., Valverde, M.A. and INESTROSA,
N.C. (2002). “Vitamin
E but not 17 _-estradiol protects against vascular toxicity
induced by _-amyloid wild type and the Dutch amyloid variant”.
J. Neurosc. 22: 3081-3089.
Opazo, C., Huang, X., Cherny, R.A., Moir,
R.D., Roher, A.E., White, A. R., Cappa, R., Masters, C.L.,
Tanzi, R.E., INESTROSA, N.C. and Bush, A.I. (2002).
“Metalloenzyme-like activity of Alzheimer’s disease _-amyloid”.
J. Biol. Chem 277: 40302-40308. |
|
