PT  - JOURNAL ARTICLE
AU  - Tajima, K.
AU  - Kawanami, T.
AU  - Nagai, R.
AU  - Horiuchi, S.
AU  - Kato, T.
TI  - Hereditary ceruloplasmin deficiency increases advanced glycation end products in the brain
AID  - 10.1212/WNL.53.3.619
DP  - 1999 Aug 01
TA  - Neurology
PG  - 619--619
VI  - 53
IP  - 3
4099  - http://n.neurology.org/content/53/3/619.short
4100  - http://n.neurology.org/content/53/3/619.full
SO  - Neurology1999 Aug 01; 53
AB  - Article abstract We investigated the role of ceruloplasmin in the antioxidative process in the brain in a patient with hereditary ceruloplasmin deficiency (HCD). Immunohistochemistry revealed an accumulation of Nε-(carboxymethyl) lysine (CML) in basal ganglia of the HCD brain. In vitro study disclosed that ceruloplasmin inhibited CML formation from glycated proteins through the reaction of Fe2+ with H2O2 by Fenton reaction. These data suggest that ceruloplasmin plays an important role in the protection of neurons against oxidative stress associated with iron metabolism.