Vijay Kumar1, Ashok Kumar2, Kritanjali Singh3, Kapil Avasthi2, Jong-Joo Kim4. 1. Department of Biotechnology, Yeungnam University, Gyeongsan, Gyeongbuk, 38541, Republic of Korea. vijaykumarcbt@gmail.com. 2. Department of Genetics, Sanjay Gandhi Post-Graduate Institute of Medical Sciences, Lucknow, 226014, UP, India. 3. Central Research Station, Subharti Medical College, Swami Vivekanand Subharti University, Meerut, 250002, India. 4. Department of Biotechnology, Yeungnam University, Gyeongsan, Gyeongbuk, 38541, Republic of Korea. kimjj@ynu.ac.kr.
Abstract
BACKGROUND: Zinc (Zn) has a diverse role in many biological processes, such as growth, immunity, anti-oxidation system, homeostatic, and repairing. It acts as a regulatory and structural catalyst ion for activities of various proteins, enzymes, and signal transcription factors, as well as cell proliferation, differentiation, and survival. The Zn ion is essential for neuronal signaling and is mainly distributed within presynaptic vesicles. Zn modulates neuronal plasticity and synaptic activity in both neonatal and adult stages. Alterations in brain Zn status results in a dozen neurological diseases including impaired brain development. Numerous researchers are working on neurogenesis, however, there is a paucity of knowledge about neurogenesis, especially in neurogenesis in adults. Neurogenesis is a multifactorial process and is regulated by many metal ions (e.g. Fe, Cu, Zn, etc.). Among them, Zn has an essential role in neurogenesis. At the molecular level, Zn controls cell cycle, apoptosis, and binding of DNA and several proteins including transcriptional and translational factors. Zn is needed for protein folding and function and Zn acts as an anti-apoptotic agent; organelle stabilizer; and an anti-inflammatory agent. Zn deficiency results in aging, neurodegenerative disease, immune deficiency, abnormal growth, cancer, and other symptoms. Prenatal deficiency of Zn results in developmental disorders in humans and animals. CONCLUSION: Both in vitro and in vivo studies have shown an association between Zn deficiency and increased risk of neurological disorders. This article reviews the existing knowledge on the role of Zn and its importance in neurogenesis.
BACKGROUND: Zinc (Zn) has a diverse role in many biological processes, such as growth, immunity, anti-oxidation system, homeostatic, and repairing. It acts as a regulatory and structural catalyst ion for activities of various proteins, enzymes, and signal transcription factors, as well as cell proliferation, differentiation, and survival. The Zn ion is essential for neuronal signaling and is mainly distributed within presynaptic vesicles. Zn modulates neuronal plasticity and synaptic activity in both neonatal and adult stages. Alterations in brain Zn status results in a dozen neurological diseases including impaired brain development. Numerous researchers are working on neurogenesis, however, there is a paucity of knowledge about neurogenesis, especially in neurogenesis in adults. Neurogenesis is a multifactorial process and is regulated by many metal ions (e.g. Fe, Cu, Zn, etc.). Among them, Zn has an essential role in neurogenesis. At the molecular level, Zn controls cell cycle, apoptosis, and binding of DNA and several proteins including transcriptional and translational factors. Zn is needed for protein folding and function and Zn acts as an anti-apoptotic agent; organelle stabilizer; and an anti-inflammatory agent. Zn deficiency results in aging, neurodegenerative disease, immune deficiency, abnormal growth, cancer, and other symptoms. Prenatal deficiency of Zn results in developmental disorders in humans and animals. CONCLUSION: Both in vitro and in vivo studies have shown an association between Zn deficiency and increased risk of neurological disorders. This article reviews the existing knowledge on the role of Zn and its importance in neurogenesis.
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