Neonatal Hypoxia Ischaemia: Mechanisms, Models, and Therapeutic Challenges

Neonatal hypoxia-ischaemia (HI) is the most common cause of death and disability in human neonates, and is often associated with persistent motor, sensory, and cognitive impairment. Improved intensive care technology has increased survival without preventing neurological disorder, increasing morbidi...

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Main Authors: Millar, L, Shi, L, Hoerder-Suabedissen, A, Molnár, Z
Format: Journal article
Language:English
Published: Frontiers Media S.A. 2017
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author Millar, L
Shi, L
Hoerder-Suabedissen, A
Molnár, Z
author_facet Millar, L
Shi, L
Hoerder-Suabedissen, A
Molnár, Z
author_sort Millar, L
collection OXFORD
description Neonatal hypoxia-ischaemia (HI) is the most common cause of death and disability in human neonates, and is often associated with persistent motor, sensory, and cognitive impairment. Improved intensive care technology has increased survival without preventing neurological disorder, increasing morbidity throughout the adult population. Early preventative or neuroprotective interventions have the potential to rescue brain development in neonates, yet only one therapeutic intervention is currently licensed for use in developed countries. Recent investigations of the transient cortical layer known as subplate, especially regarding subplate's secretory role, opens up a novel set of potential molecular modulators of neonatal HI injury. This review examines the biological mechanisms of human neonatal HI, discusses evidence for the relevance of subplate-secreted molecules to this condition, and evaluates available animal models. Neuroserpin, a neuronally released neuroprotective factor, is discussed as a case study for developing new potential pharmacological interventions for use post-ischaemic injury.
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spelling oxford-uuid:88c0a873-6300-4b47-a076-26cf4dcf09372022-03-26T22:19:37ZNeonatal Hypoxia Ischaemia: Mechanisms, Models, and Therapeutic ChallengesJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:88c0a873-6300-4b47-a076-26cf4dcf0937EnglishSymplectic Elements at OxfordFrontiers Media S.A.2017Millar, LShi, LHoerder-Suabedissen, AMolnár, ZNeonatal hypoxia-ischaemia (HI) is the most common cause of death and disability in human neonates, and is often associated with persistent motor, sensory, and cognitive impairment. Improved intensive care technology has increased survival without preventing neurological disorder, increasing morbidity throughout the adult population. Early preventative or neuroprotective interventions have the potential to rescue brain development in neonates, yet only one therapeutic intervention is currently licensed for use in developed countries. Recent investigations of the transient cortical layer known as subplate, especially regarding subplate's secretory role, opens up a novel set of potential molecular modulators of neonatal HI injury. This review examines the biological mechanisms of human neonatal HI, discusses evidence for the relevance of subplate-secreted molecules to this condition, and evaluates available animal models. Neuroserpin, a neuronally released neuroprotective factor, is discussed as a case study for developing new potential pharmacological interventions for use post-ischaemic injury.
spellingShingle Millar, L
Shi, L
Hoerder-Suabedissen, A
Molnár, Z
Neonatal Hypoxia Ischaemia: Mechanisms, Models, and Therapeutic Challenges
title Neonatal Hypoxia Ischaemia: Mechanisms, Models, and Therapeutic Challenges
title_full Neonatal Hypoxia Ischaemia: Mechanisms, Models, and Therapeutic Challenges
title_fullStr Neonatal Hypoxia Ischaemia: Mechanisms, Models, and Therapeutic Challenges
title_full_unstemmed Neonatal Hypoxia Ischaemia: Mechanisms, Models, and Therapeutic Challenges
title_short Neonatal Hypoxia Ischaemia: Mechanisms, Models, and Therapeutic Challenges
title_sort neonatal hypoxia ischaemia mechanisms models and therapeutic challenges
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AT shil neonatalhypoxiaischaemiamechanismsmodelsandtherapeuticchallenges
AT hoerdersuabedissena neonatalhypoxiaischaemiamechanismsmodelsandtherapeuticchallenges
AT molnarz neonatalhypoxiaischaemiamechanismsmodelsandtherapeuticchallenges