Math P. Cuajungco

Dr. Math P. Cuajungco

California State University Fullerton
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Research Focus & Metrics

Academic Career Length

31Years (1996-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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27 May 1999 in Biochemistry
Verified
Journal Article
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XHXudong Huang
Xudong Huang
CACraig S. Atwood
Craig S. Atwood
MHMariana A. Hartshorn
Mariana A. Hartshorn
GMGerd Multhaup
Gerd Multhaup
LGLee E. Goldstein
Lee E. Goldstein
Ashley I. BushAshley I. Bush
Ashley I. Bush

1 December 1999 in Journal of Biological Chemistry
Verified
Journal Article
Open access
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XHXudong Huang
Xudong Huang
Math P. CuajungcoMath P. Cuajungco
Math P. Cuajungco
CACraig S. Atwood
Craig S. Atwood
MHMariana A. Hartshorn
Mariana A. Hartshorn
Joel TyndallJoel Tyndall
Joel Tyndall
Ashley I. BushAshley I. Bush
Ashley I. Bush
Oxidative stress markers as well as high concentrations of copper are found in the vicinity of Aβ amyloid deposits in Alzheimer's disease. The neurotoxicity of Aβ in cell culture has been linked to H2O2generation by an unknown mechanism. We now report that Cu(II) markedly potentiates the neurotoxicity exhibited by Aβ in cell culture. The potentiation of toxicity is greatest for Aβ1–42 > Aβ1–40 ≫ mouse/rat Aβ1–40, corresponding to their relative capacities to reduce Cu(II) to Cu(I), form H2O2 in cell-free assays and to exhibit amyloid pathology. The copper complex of Aβ1–42 has a highly positive formal reduction potential (≈+500–550 mV versus Ag/AgCl) characteristic of strongly reducing cuproproteins. These findings suggest that certain redox active metal ions may be important in exacerbating and perhaps facilitating Aβ-mediated oxidative damage in Alzheimer's disease.

1 March 2001 in The American Journal of Human Genetics
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Journal Article
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SSSusan A. Slaugenhaupt
Susan A. Slaugenhaupt
ABAnat Blumenfeld
Anat Blumenfeld
SGSandra P. Gill
Sandra P. Gill
MLMaire Leyne
Maire Leyne
JMJames Mull
James Mull
JGJames F. Gusella
James F. Gusella

1 January 1997 in Neurobiology of Disease
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Journal Article
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Math P. CuajungcoMath P. Cuajungco
Math P. Cuajungco
GLGordon J. Lees
Gordon J. Lees

1 June 2000 in Journal of Biological Chemistry
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Journal Article
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Math P. CuajungcoMath P. Cuajungco
Math P. Cuajungco
LGLee E. Goldstein
Lee E. Goldstein
ANAkihiko Nunomura
Akihiko Nunomura
MSMark A. Smith
Mark A. Smith
JLJames T. Lim
James T. Lim
Ashley I. BushAshley I. Bush
Ashley I. Bush
Aβ binds Zn2+, Cu2+, and Fe3+ in vitro, and these metals are markedly elevated in the neocortex and especially enriched in amyloid plaque deposits of individuals with Alzheimer's disease (AD). Zn2+ precipitates Aβ in vitro, and Cu2+ interaction with Aβ promotes its neurotoxicity, correlating with metal reduction and the cell-free generation of H2O2 (Aβ1–42 > Aβ1–40 > ratAβ1–40). Because Zn2+ is redox-inert, we studied the possibility that it may play an inhibitory role in H2O2-mediated Aβ toxicity. In competition to the cytotoxic potentiation caused by coincubation with Cu2+, Zn2+ rescued primary cortical and human embryonic kidney 293 cells that were exposed to Aβ1–42, correlating with the effect of Zn2+ in suppressing Cu2+-dependent H2O2formation from Aβ1–42. Since plaques contain exceptionally high concentrations of Zn2+, we examined the relationship between oxidation (8-OH guanosine) levels in AD-affected tissue and histological amyloid burden and found a significant negative correlation. These data suggest a protective role for Zn2+in AD, where plaques form as the result of a more robust Zn2+ antioxidant response to the underlying oxidative attack.

1 January 2003 in Brain Research Reviews
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Journal Article
Closed access
Math P. CuajungcoMath P. Cuajungco
Math P. Cuajungco
KFKyle Y. Fagét
Kyle Y. Fagét