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Neuroprotective therapies after perinatal hypoxic-ischemic brain injury.

Cerio FG, Lara-Celador I, Alvarez A, Hilario E - Brain Sci (2013)

Bottom Line: It is the result of a deprivation of oxygen and glucose in the neural tissue.The pattern of this injury occurs in two phases, the first one is a primary energy failure related to the HI event and the second phase is an energy failure that takes place some hours later.Injuries that occur in response to these events are often manifested as severe cognitive and motor disturbances over time.

View Article: PubMed Central - PubMed

Affiliation: Biotechnology Area, GAIKER Technology Centre, Parque Tecnológico de Zamudio Ed 202, 48170 Zamudio, Vizcaya, Spain. goni@gaiker.es.

ABSTRACT
Hypoxic-ischemic (HI) brain injury is one of the main causes of disabilities in term-born infants. It is the result of a deprivation of oxygen and glucose in the neural tissue. As one of the most important causes of brain damage in the newborn period, the neonatal HI event is a devastating condition that can lead to long-term neurological deficits or even death. The pattern of this injury occurs in two phases, the first one is a primary energy failure related to the HI event and the second phase is an energy failure that takes place some hours later. Injuries that occur in response to these events are often manifested as severe cognitive and motor disturbances over time. Due to difficulties regarding the early diagnosis and treatment of HI injury, there is an increasing need to find effective therapies as new opportunities for the reduction of brain damage and its long term effects. Some of these therapies are focused on prevention of the production of reactive oxygen species, anti-inflammatory effects, anti-apoptotic interventions and in a later stage, the stimulation of neurotrophic properties in the neonatal brain which could be targeted to promote neuronal and oligodendrocyte regeneration.

No MeSH data available.


Related in: MedlinePlus

Cascade of biochemical mechanism after hypoxic-ischemic (HI) brain injury. A schematic diagram that summarizes the cellular and molecular events triggered after HI injury in the developing brain. Mitochondrial damage, the cytotoxic levels of intracellular calcium and the release of inflammatory mediators cause metabolic failure, oxidative stress and ultimately the cell death.
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brainsci-03-00191-f001: Cascade of biochemical mechanism after hypoxic-ischemic (HI) brain injury. A schematic diagram that summarizes the cellular and molecular events triggered after HI injury in the developing brain. Mitochondrial damage, the cytotoxic levels of intracellular calcium and the release of inflammatory mediators cause metabolic failure, oxidative stress and ultimately the cell death.

Mentions: Brain damage following a perinatal HI is an evolving process, which is comprised of two phases [13]. A first phase consists of an early energetic failure, where the oxidative energy metabolism of cells decreases and it promotes necrotic death. This is followed by a second phase of cell death, a late energetic failure, which occurs during reperfusion and reoxygenation several hours after the initial event and lasts for days [10,22,23]. The pathophysiology of this late energetic failure initiates a cascade of biochemical events (Figure 1), which involve nitric oxide synthases activation, the production of cytotoxic free radicals, inflammation, membrane dysfunction and apoptosis, among others [24].


Neuroprotective therapies after perinatal hypoxic-ischemic brain injury.

Cerio FG, Lara-Celador I, Alvarez A, Hilario E - Brain Sci (2013)

Cascade of biochemical mechanism after hypoxic-ischemic (HI) brain injury. A schematic diagram that summarizes the cellular and molecular events triggered after HI injury in the developing brain. Mitochondrial damage, the cytotoxic levels of intracellular calcium and the release of inflammatory mediators cause metabolic failure, oxidative stress and ultimately the cell death.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4061821&req=5

brainsci-03-00191-f001: Cascade of biochemical mechanism after hypoxic-ischemic (HI) brain injury. A schematic diagram that summarizes the cellular and molecular events triggered after HI injury in the developing brain. Mitochondrial damage, the cytotoxic levels of intracellular calcium and the release of inflammatory mediators cause metabolic failure, oxidative stress and ultimately the cell death.
Mentions: Brain damage following a perinatal HI is an evolving process, which is comprised of two phases [13]. A first phase consists of an early energetic failure, where the oxidative energy metabolism of cells decreases and it promotes necrotic death. This is followed by a second phase of cell death, a late energetic failure, which occurs during reperfusion and reoxygenation several hours after the initial event and lasts for days [10,22,23]. The pathophysiology of this late energetic failure initiates a cascade of biochemical events (Figure 1), which involve nitric oxide synthases activation, the production of cytotoxic free radicals, inflammation, membrane dysfunction and apoptosis, among others [24].

Bottom Line: It is the result of a deprivation of oxygen and glucose in the neural tissue.The pattern of this injury occurs in two phases, the first one is a primary energy failure related to the HI event and the second phase is an energy failure that takes place some hours later.Injuries that occur in response to these events are often manifested as severe cognitive and motor disturbances over time.

View Article: PubMed Central - PubMed

Affiliation: Biotechnology Area, GAIKER Technology Centre, Parque Tecnológico de Zamudio Ed 202, 48170 Zamudio, Vizcaya, Spain. goni@gaiker.es.

ABSTRACT
Hypoxic-ischemic (HI) brain injury is one of the main causes of disabilities in term-born infants. It is the result of a deprivation of oxygen and glucose in the neural tissue. As one of the most important causes of brain damage in the newborn period, the neonatal HI event is a devastating condition that can lead to long-term neurological deficits or even death. The pattern of this injury occurs in two phases, the first one is a primary energy failure related to the HI event and the second phase is an energy failure that takes place some hours later. Injuries that occur in response to these events are often manifested as severe cognitive and motor disturbances over time. Due to difficulties regarding the early diagnosis and treatment of HI injury, there is an increasing need to find effective therapies as new opportunities for the reduction of brain damage and its long term effects. Some of these therapies are focused on prevention of the production of reactive oxygen species, anti-inflammatory effects, anti-apoptotic interventions and in a later stage, the stimulation of neurotrophic properties in the neonatal brain which could be targeted to promote neuronal and oligodendrocyte regeneration.

No MeSH data available.


Related in: MedlinePlus