Your browser doesn't support javascript.
loading
A possible significant role of zinc and GPR39 zinc sensing receptor in Alzheimer disease and epilepsy.
Khan, Muhammad Zahid.
Afiliação
  • Khan MZ; Department of Pharmacology, China Pharmaceutical University, Nanjing 210009, China. Electronic address: mzahidk786@hotmail.com.
Biomed Pharmacother ; 79: 263-72, 2016 Apr.
Article em En | MEDLINE | ID: mdl-27044837
ABSTRACT
Zinc the essential trace element, plays a significant role in the brain development and in the proper brain functions at every stage of life. Misbalance of zinc (Zn(2+)) ions in the central nervous system is involved in the pathogenesis of numerous neurodegenerative disorders such as Alzheimer's disease, Depression, and Epilepsy. In brain, Zn(2+) has been identified as a ligand, capable of activating and inhibiting the receptors including the NMDA-type glutamate receptors (NMDARs), GABAA receptors, nicotinic acetylcholine receptors (nAChRs), glycine receptors (glyR) and serotonin receptors (5-HT3). Recently GPR39 has been identified as a zinc-specific receptor, widely expressed in brain tissues including the frontal cortex, amygdala, and hippocampus. GPR39, when binding with Zn(2+) has shown promising therapeutic potentials. This review presents current knowledge regarding the role of GPR39 zinc sensing receptor in brain, with a focus on Alzheimer's disease and Epilepsy. Although the results are encouraging, further research is needed to clarify zinc and GPR39 role in the treatment of Alzheimer's disease and Epilepsy.
Assuntos
Palavras-chave

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Zinco / Receptores Acoplados a Proteínas G / Epilepsia / Doença de Alzheimer Limite: Animals / Humans Idioma: En Revista: Biomed Pharmacother Ano de publicação: 2016 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Zinco / Receptores Acoplados a Proteínas G / Epilepsia / Doença de Alzheimer Limite: Animals / Humans Idioma: En Revista: Biomed Pharmacother Ano de publicação: 2016 Tipo de documento: Article