Preterm newborns represent a high-risk population for brain damage, primarily affecting the white matter, and for related neurodevelopmental disabilities. Determinants of brain damage have been extensively investigated, but there are still many controversies on how these factors can influence the developing brain and provoke damage. The concept of etiological pathway, instead of a single determinant, appears to better explain pathogenetic mechanisms: the brain damage may represent the final outcome of exposure to several combinations of risk factors in the same pathway or in different pathways and can change according to the gestational age. The aim of this article is to review the current knowledge on the pathogenesis of brain damage in preterm infants, within the frame of two main theoretical models, the ischemic and the inflammatory pathway. The relationship between the two pathways and the contribution of genetic susceptibility to ischemic and/or inflammatory insult, in modulating the extent and severity of brain damage, is also discussed.
%0 Journal Article
%1 Arpino2005
%A Arpino, Carla
%A D'Argenzio, Luigi
%A Ticconi, Carlo
%A Paolo, Ambrogio Di
%A Stellin, Vincenzo
%A Lopez, Luisa
%A Curatolo, Paolo
%D 2005
%J Ann Ist Super Sanita
%K Adult; Birth Injuries; Brain Damage, Chronic; Cerebral P; Chorioamnionitis; Cytokines; Developmental Disabilities; Epilepsy; Female; Fetal Diseases; Hypoxia; Genetic Predisposition to Disease; Humans; Hypoxia-Ischemia, Brain; Infant, Low Weight; Newborn; Premature; Inflammation Mediators; Learning Disorders; Male; Mental Retardation; Models, Neurological; Pregnancy; Pregnancy Complications; Prenatal Exposure Delayed Effects; Risk Factors; alsy
%N 2
%P 229--237
%T Brain damage in preterm infants: etiological pathways.
%V 41
%X Preterm newborns represent a high-risk population for brain damage, primarily affecting the white matter, and for related neurodevelopmental disabilities. Determinants of brain damage have been extensively investigated, but there are still many controversies on how these factors can influence the developing brain and provoke damage. The concept of etiological pathway, instead of a single determinant, appears to better explain pathogenetic mechanisms: the brain damage may represent the final outcome of exposure to several combinations of risk factors in the same pathway or in different pathways and can change according to the gestational age. The aim of this article is to review the current knowledge on the pathogenesis of brain damage in preterm infants, within the frame of two main theoretical models, the ischemic and the inflammatory pathway. The relationship between the two pathways and the contribution of genetic susceptibility to ischemic and/or inflammatory insult, in modulating the extent and severity of brain damage, is also discussed.
@article{Arpino2005,
abstract = {Preterm newborns represent a high-risk population for brain damage, primarily affecting the white matter, and for related neurodevelopmental disabilities. Determinants of brain damage have been extensively investigated, but there are still many controversies on how these factors can influence the developing brain and provoke damage. The concept of etiological pathway, instead of a single determinant, appears to better explain pathogenetic mechanisms: the brain damage may represent the final outcome of exposure to several combinations of risk factors in the same pathway or in different pathways and can change according to the gestational age. The aim of this article is to review the current knowledge on the pathogenesis of brain damage in preterm infants, within the frame of two main theoretical models, the ischemic and the inflammatory pathway. The relationship between the two pathways and the contribution of genetic susceptibility to ischemic and/or inflammatory insult, in modulating the extent and severity of brain damage, is also discussed.},
added-at = {2014-07-19T17:42:51.000+0200},
author = {Arpino, Carla and D'Argenzio, Luigi and Ticconi, Carlo and Paolo, Ambrogio Di and Stellin, Vincenzo and Lopez, Luisa and Curatolo, Paolo},
biburl = {https://www.bibsonomy.org/bibtex/2bcf1b688658e4ef42a09d8cdec650d76/ar0berts},
groups = {public},
interhash = {9c32817ac2a24d8cf524f2ed8e95d27e},
intrahash = {bcf1b688658e4ef42a09d8cdec650d76},
journal = {Ann Ist Super Sanita},
keywords = {Adult; Birth Injuries; Brain Damage, Chronic; Cerebral P; Chorioamnionitis; Cytokines; Developmental Disabilities; Epilepsy; Female; Fetal Diseases; Hypoxia; Genetic Predisposition to Disease; Humans; Hypoxia-Ischemia, Brain; Infant, Low Weight; Newborn; Premature; Inflammation Mediators; Learning Disorders; Male; Mental Retardation; Models, Neurological; Pregnancy; Pregnancy Complications; Prenatal Exposure Delayed Effects; Risk Factors; alsy},
number = 2,
pages = {229--237},
pmid = {16244398},
timestamp = {2014-07-19T17:42:51.000+0200},
title = {Brain damage in preterm infants: etiological pathways.},
username = {ar0berts},
volume = 41,
year = 2005
}