TY - JOUR
T1 - Copper and the brain noradrenergic system
AU - Lutsenko, Svetlana
AU - Washington-Hughes, Clorissa
AU - Ralle, Martina
AU - Schmidt, Katharina
N1 - Funding Information:
This work was supported by the National Institute of Health Grant R01 GM101502 to SL and R01 GM101502-S1 to CWH. The authors would like to thank O. Antipova for support and assistance with X-ray fluorescence microscopy data collection at the Advanced Photon Source part of the Argonne National laboratory supported by the Department of Energy, Office of Basic Energy Sciences, under contract no. DE-AC02-06CH11357.
Funding Information:
This work was supported by the National Institute of Health Grant R01 GM101502 to SL and R01 GM101502-S1 to CWH. The authors would like to thank O. Antipova for support and assistance with X-ray fluorescence microscopy data collection at the Advanced Photon Source part of the Argonne National laboratory supported by the Department of Energy, Office of Basic Energy Sciences, under contract no. DE-AC02-06CH11357.
Publisher Copyright:
© 2019, Society for Biological Inorganic Chemistry (SBIC).
PY - 2019/12/1
Y1 - 2019/12/1
N2 - Copper (Cu) plays an essential role in the development and function of the brain. In humans, genetic disorders of Cu metabolism may cause either severe Cu deficiency (Menkes disease) or excessive Cu accumulation (Wilson disease) in the brain tissue. In either case, the loss of Cu homeostasis results in catecholamine misbalance, abnormal myelination of neurons, loss of normal brain architecture, and a spectrum of neurologic and/or psychiatric manifestations. Several metabolic processes have been identified as particularly sensitive to Cu dis-homeostasis. This review focuses on the role of Cu in noradrenergic neurons and summarizes the current knowledge of mechanisms that maintain Cu homeostasis in these cells. The impact of Cu misbalance on catecholamine metabolism and functioning of noradrenergic system is discussed.
AB - Copper (Cu) plays an essential role in the development and function of the brain. In humans, genetic disorders of Cu metabolism may cause either severe Cu deficiency (Menkes disease) or excessive Cu accumulation (Wilson disease) in the brain tissue. In either case, the loss of Cu homeostasis results in catecholamine misbalance, abnormal myelination of neurons, loss of normal brain architecture, and a spectrum of neurologic and/or psychiatric manifestations. Several metabolic processes have been identified as particularly sensitive to Cu dis-homeostasis. This review focuses on the role of Cu in noradrenergic neurons and summarizes the current knowledge of mechanisms that maintain Cu homeostasis in these cells. The impact of Cu misbalance on catecholamine metabolism and functioning of noradrenergic system is discussed.
KW - Catecholamines
KW - Copper
KW - Dopamine-β-hydroxylase
KW - Locus coeruleus
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U2 - 10.1007/s00775-019-01737-3
DO - 10.1007/s00775-019-01737-3
M3 - Review article
C2 - 31691104
AN - SCOPUS:85074794836
SN - 0949-8257
VL - 24
SP - 1179
EP - 1188
JO - Journal of Biological Inorganic Chemistry
JF - Journal of Biological Inorganic Chemistry
IS - 8
ER -