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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

Neuroprotective therapies and their optimal moment of administration, according to their mechanisms of action. In this sense, pharmacological antioxidant therapies such as melatonin, allopurinol, hypothermia or magnesium sulfate could be useful just after the HI event. After the reperfusion, when the secondary energy failure takes place, other therapeutic options like cannabinoids, erythropoietin or iminobiotin, which have anti-inflammation and anti-apoptotic effects, could be promising therapies.
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brainsci-03-00191-f002: Neuroprotective therapies and their optimal moment of administration, according to their mechanisms of action. In this sense, pharmacological antioxidant therapies such as melatonin, allopurinol, hypothermia or magnesium sulfate could be useful just after the HI event. After the reperfusion, when the secondary energy failure takes place, other therapeutic options like cannabinoids, erythropoietin or iminobiotin, which have anti-inflammation and anti-apoptotic effects, could be promising therapies.

Mentions: Many potential neuroprotective therapies that target specific pathways in the pathophysiology of HI brain injury have been investigated. At present, no individual neuroprotective agents have been proven safe and effective against neurological sequels after HI events in neonates. The insight into the biochemical and cellular mechanisms of neuronal injury after HI helps to provide interventions to interrupt those deleterious cascades derived from the event [49]. Pharmacological and non pharmacological therapies should start at different points of time after the HI event, in their optimal therapeutic window, according to their mechanisms of action (Figure 2). Moreover, some of these therapies are supplied pre-HI event. Anyway, the goals of these therapies are: reduce cerebral damage by decreasing the formation of toxic free-radicals, inhibit the excessive influx of calcium into neurons and minimize cerebral edema principally [50,51].


Neuroprotective therapies after perinatal hypoxic-ischemic brain injury.

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

Neuroprotective therapies and their optimal moment of administration, according to their mechanisms of action. In this sense, pharmacological antioxidant therapies such as melatonin, allopurinol, hypothermia or magnesium sulfate could be useful just after the HI event. After the reperfusion, when the secondary energy failure takes place, other therapeutic options like cannabinoids, erythropoietin or iminobiotin, which have anti-inflammation and anti-apoptotic effects, could be promising therapies.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

brainsci-03-00191-f002: Neuroprotective therapies and their optimal moment of administration, according to their mechanisms of action. In this sense, pharmacological antioxidant therapies such as melatonin, allopurinol, hypothermia or magnesium sulfate could be useful just after the HI event. After the reperfusion, when the secondary energy failure takes place, other therapeutic options like cannabinoids, erythropoietin or iminobiotin, which have anti-inflammation and anti-apoptotic effects, could be promising therapies.
Mentions: Many potential neuroprotective therapies that target specific pathways in the pathophysiology of HI brain injury have been investigated. At present, no individual neuroprotective agents have been proven safe and effective against neurological sequels after HI events in neonates. The insight into the biochemical and cellular mechanisms of neuronal injury after HI helps to provide interventions to interrupt those deleterious cascades derived from the event [49]. Pharmacological and non pharmacological therapies should start at different points of time after the HI event, in their optimal therapeutic window, according to their mechanisms of action (Figure 2). Moreover, some of these therapies are supplied pre-HI event. Anyway, the goals of these therapies are: reduce cerebral damage by decreasing the formation of toxic free-radicals, inhibit the excessive influx of calcium into neurons and minimize cerebral edema principally [50,51].

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