Jovanović, Saša

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  • Jovanović, Saša (1)
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Molecular basis of brain injury and repair

Peković, Sanja; Dacić, Sanja; Nedeljković, Nadežda; Bjelobaba, Ivana; Filipović, Radmila; Milenković, Ivan; Lavrnja, Irena; Savić, Danijela; Jovanović, Saša; Rakić, Ljubisav; Stojiljković, Mirjana

(Kerala, India: Research Signpost, 2006)

TY  - CHAP
AU  - Peković, Sanja
AU  - Dacić, Sanja
AU  - Nedeljković, Nadežda
AU  - Bjelobaba, Ivana
AU  - Filipović, Radmila
AU  - Milenković, Ivan
AU  - Lavrnja, Irena
AU  - Savić, Danijela
AU  - Jovanović, Saša
AU  - Rakić, Ljubisav
AU  - Stojiljković, Mirjana
PY  - 2006
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5871
AB  - Injury to the central nervous system (CNS) is one of the leading causes of death and invalidity among all people below the age of 45 for which there are no specific treatments. The insight into the molecular pathophysiology of brain dysfunctions after the injury will provide indications for new effective therapeutic approaches that will limit damage, slow cell death and promote repair. The aim of this review is to highlight molecular mechanisms underlining primary and secondary injury. The initial impact or primary injury induces elevation of extracellular concentration of neurotransmitters leading to changes in electrical properties of neuronal membrane, net influx of Ca2+ and activation of diverse cellular signaling pathways. To restore neuronal homeostasis, the activities and expression of a variety of enzymes involved in control of extracellular concentration of biogenic amines and purine nucleotides/nucleosides, as well as the membrane potential are altered. The CNS has a limited capacity of self-repair. However, there are indications that the neonatal brain has a greater capacity for recovery than adult brain. The well known pathological hallmark of CNS injury is formation of the glial scar, the major impediment to axonal regeneration. Recently, it was shown that treatment with the purine nucleoside analogues attenuates and delays the process of reactive gliosis, and thus may be a useful approach for improving neurological recovery from head injury.
PB  - Kerala, India: Research Signpost
T2  - Neurobiological studies – From genes to behavior 2006
T1  - Molecular basis of brain injury and repair
SP  - 143
EP  - 165
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5871
ER  - 
@inbook{
author = "Peković, Sanja and Dacić, Sanja and Nedeljković, Nadežda and Bjelobaba, Ivana and Filipović, Radmila and Milenković, Ivan and Lavrnja, Irena and Savić, Danijela and Jovanović, Saša and Rakić, Ljubisav and Stojiljković, Mirjana",
year = "2006",
abstract = "Injury to the central nervous system (CNS) is one of the leading causes of death and invalidity among all people below the age of 45 for which there are no specific treatments. The insight into the molecular pathophysiology of brain dysfunctions after the injury will provide indications for new effective therapeutic approaches that will limit damage, slow cell death and promote repair. The aim of this review is to highlight molecular mechanisms underlining primary and secondary injury. The initial impact or primary injury induces elevation of extracellular concentration of neurotransmitters leading to changes in electrical properties of neuronal membrane, net influx of Ca2+ and activation of diverse cellular signaling pathways. To restore neuronal homeostasis, the activities and expression of a variety of enzymes involved in control of extracellular concentration of biogenic amines and purine nucleotides/nucleosides, as well as the membrane potential are altered. The CNS has a limited capacity of self-repair. However, there are indications that the neonatal brain has a greater capacity for recovery than adult brain. The well known pathological hallmark of CNS injury is formation of the glial scar, the major impediment to axonal regeneration. Recently, it was shown that treatment with the purine nucleoside analogues attenuates and delays the process of reactive gliosis, and thus may be a useful approach for improving neurological recovery from head injury.",
publisher = "Kerala, India: Research Signpost",
journal = "Neurobiological studies – From genes to behavior 2006",
booktitle = "Molecular basis of brain injury and repair",
pages = "143-165",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5871"
}
Peković, S., Dacić, S., Nedeljković, N., Bjelobaba, I., Filipović, R., Milenković, I., Lavrnja, I., Savić, D., Jovanović, S., Rakić, L.,& Stojiljković, M.. (2006). Molecular basis of brain injury and repair. in Neurobiological studies – From genes to behavior 2006
Kerala, India: Research Signpost., 143-165.
https://hdl.handle.net/21.15107/rcub_ibiss_5871
Peković S, Dacić S, Nedeljković N, Bjelobaba I, Filipović R, Milenković I, Lavrnja I, Savić D, Jovanović S, Rakić L, Stojiljković M. Molecular basis of brain injury and repair. in Neurobiological studies – From genes to behavior 2006. 2006;:143-165.
https://hdl.handle.net/21.15107/rcub_ibiss_5871 .
Peković, Sanja, Dacić, Sanja, Nedeljković, Nadežda, Bjelobaba, Ivana, Filipović, Radmila, Milenković, Ivan, Lavrnja, Irena, Savić, Danijela, Jovanović, Saša, Rakić, Ljubisav, Stojiljković, Mirjana, "Molecular basis of brain injury and repair" in Neurobiological studies – From genes to behavior 2006 (2006):143-165,
https://hdl.handle.net/21.15107/rcub_ibiss_5871 .
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