TY - JOUR
T1 - Dihydropteridine reductase activity
T2 - Lack of association with serum aluminum levels and cognitive functioning in patients with end–stage renal disease
AU - Bolla, K. I.
AU - Milstien, S.
AU - Briefel, G.
AU - Wieler, L.
AU - Kaufman, S.
PY - 1991/11
Y1 - 1991/11
N2 - Although increased levels of aluminum (Al) are present in patients with dialysis encephalopathy (DE), it is unclear if the association is causal. The enzyme dihydropteridine reductase (DHPR) plays a critical role in neurotransmitter formation and its activity. Elevated levels of Al are reported to decrease DHPR activity, which would alter neurotransmitter metabolism, thus producing DE. We examined the association between erythrocyte DHPR activity and Al levels, attention/psychomotor skills, and depression in a group of 21 patients with end-stage renal disease. DHPR activity was not related to Al level, mental status, psychomotor ability, or depression score. After administration of deferoxamine (an Al chelating agent), Al level increased significantly but DHPR activity remained the same. Our results suggest that the mechanism for the development for DE does not involve alterations of neurotransmitter metabolism caused by Al-mediated reductions in DHPR activity.
AB - Although increased levels of aluminum (Al) are present in patients with dialysis encephalopathy (DE), it is unclear if the association is causal. The enzyme dihydropteridine reductase (DHPR) plays a critical role in neurotransmitter formation and its activity. Elevated levels of Al are reported to decrease DHPR activity, which would alter neurotransmitter metabolism, thus producing DE. We examined the association between erythrocyte DHPR activity and Al levels, attention/psychomotor skills, and depression in a group of 21 patients with end-stage renal disease. DHPR activity was not related to Al level, mental status, psychomotor ability, or depression score. After administration of deferoxamine (an Al chelating agent), Al level increased significantly but DHPR activity remained the same. Our results suggest that the mechanism for the development for DE does not involve alterations of neurotransmitter metabolism caused by Al-mediated reductions in DHPR activity.
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U2 - 10.1212/wnl.41.11.1806
DO - 10.1212/wnl.41.11.1806
M3 - Article
C2 - 1944913
AN - SCOPUS:0026002367
SN - 0028-3878
VL - 41
SP - 1806
EP - 1809
JO - Neurology
JF - Neurology
IS - 11
ER -