Molecular mechanisms of neonatal brain injury and neural rescue

TY - CHAP

T1 - Molecular mechanisms of neonatal brain injury and neural rescue

AU - Gressens, Pierre

AU - Hagberg, Henrik

PY - 2011/1/1

Y1 - 2011/1/1

N2 - Perinatal brain injury is a common cause of life-long neurological deficits and there is an urgent need to better understand its pathophysiology and to find strategies for prevention and treatment. The etiology is complex and multifactorial but hypoxia–ischaemia (HI), infection/inflammation and excitotoxicity (see below) are considered important causes or precipitating insults of preventable/treatable forms of perinatal brain injury. In this review, we will focus on mechanisms of brain injury in response to acute sterile insults in the developing brain that occur in term (e.g., neonatal encephalopathy) or preterm infants.Genetic background, developmental age, sex and brain maturity affect vulnerability and the mechanisms of brain injury [1,2]. Furthermore, antecedents such as infection/inflammation, intrauterine growth restriction or pre-exposures to hypoxia can modulate brain vulnerability in response to acute insults [3–5]. Brain injury evolves over time and different mechanisms are critical during the primary, secondary and tertiary phases (Figure 2.1). Indeed, recent experimental data suggest that interventions can be effective if administered hours, days or even weeks after the primary insult [6,7].

AB - Perinatal brain injury is a common cause of life-long neurological deficits and there is an urgent need to better understand its pathophysiology and to find strategies for prevention and treatment. The etiology is complex and multifactorial but hypoxia–ischaemia (HI), infection/inflammation and excitotoxicity (see below) are considered important causes or precipitating insults of preventable/treatable forms of perinatal brain injury. In this review, we will focus on mechanisms of brain injury in response to acute sterile insults in the developing brain that occur in term (e.g., neonatal encephalopathy) or preterm infants.Genetic background, developmental age, sex and brain maturity affect vulnerability and the mechanisms of brain injury [1,2]. Furthermore, antecedents such as infection/inflammation, intrauterine growth restriction or pre-exposures to hypoxia can modulate brain vulnerability in response to acute insults [3–5]. Brain injury evolves over time and different mechanisms are critical during the primary, secondary and tertiary phases (Figure 2.1). Indeed, recent experimental data suggest that interventions can be effective if administered hours, days or even weeks after the primary insult [6,7].

UR - http://www.scopus.com/inward/record.url?scp=84923619930&partnerID=8YFLogxK

U2 - 10.1017/CBO9781139565059.003

DO - 10.1017/CBO9781139565059.003

M3 - Chapter

AN - SCOPUS:84923619930

SN - 9781107681606

SP - 16

EP - 32

BT - Neonatal Neural Rescue

PB - Cambridge University Press

ER -