Neuroprotection in Brain Hypoxia

OTERO-LOSADA, M.; CAPANI F.

Frontiers in Neuroscience

Año: 2018 p. 531

978-1-873671-00-9

Neuroprotection in Brain Hypoxia and Metabolic SyndromeAlterations in blood volume and oxygen concentrations are concerning issues in worldwide healthcare. In particular, brain hypoxia-ischemia (BHI) affects not only adults but newborn infants as well, having devastating impact on health leading to costly neurological diseases and disorders. Both adults and newborns (perinatal asphyxia, PA) are affected by for BHI. Treatment outcome and rehabilitation success are strongly dependent on severity and duration of hipoxia. Neurological deficits may appear during childhood or may be delayed until overly expressed in teens or young adults. Animal models of brain hypoxia are crucial to elucidate its underlying mechanisms and to develop neuroprotective strategies and hopefully, remediation. By now, new experimental therapeutic strategies have been used and yet, only hypothermia has shown to be clinically beneficial. Lacking an established treatment for brain, neuroprotection is imperative. The understanding of PA pathophysiology contributes to the identification of neuroprotective agents. The primary insult, characterized by a severe energetic crisis, lactate accumulation and acidosis, is exacerbated during the reoxygenation period, which is associated with free radicals accumulation, oxidative stress, cell damage and inflammatory cascades. This latent phase, where secondary injury can occur, offers a therapeutic window and constitutes the basis for neuroprotection. The aim of this special issue is bringing together research studies and experimental evidence addressing the role of neuroprotective agents.Me encantó ésto!!The intended audience are mainly experts in the field and students interested in Neurobiology of Disease. With specific aims, this special issue will focuse on neuroprotective strategies for the brain, their possible pathways and the use of pharmacological agents or analogues.Potential topics include, but are not limited to:* Biochemical and physiological aspects of neuroprotection* Pathophysiological mechanisms of brain hypoxia* Pharmacological and genetic targeting strategies* Beneficial effects of neuroprotective agents on neuroplasticity and behavior* Clinical aspects of neuroprotective agents on associated damage and recovery following perinatal asphyxiaGuest EditorsLuis María García SeguraFrancisco WadonsellMATILDE OTERO-LOSADALead Editor: Prof Dr Francisco Capani, MD, PhD. Instituto de Investigaciones Cardiológicas (ININCA-UBA-CONICET), Universidad Católica Argentina (UCA) and Universidad Autónoma de Chile, Santiago, Chile. E-mail: franciscocapani@hotmail.com; fcapani@fmed.uba.arCollaborators:Dr. Eduardo Blanco Calvo, Departament de Pedagogia i Psicologia Facultat d´Educació, Psicologia i Treball Social Universitat de Lleida. e-mail: eduardo.blanco@pip.udl.catLic. Inés Herrera. ININCA (UBA-CONICET) and CIPP (UCA). e-mail: ines_herrera@uca.edu.arDr. George Barreto. Pontificia Universidad Javeriana, Colombia. e-mail: gsampaio@javeriana.edu.coDr M. Chaffanel Peláez. FEA Pediatría . UGC de Neonatología Hospital Carlos Haya. Málaga. e-mail: chuza1978@hotmail.comDr E. Hilario Department of Cell Biology and Histology, School of Medicine and Dentistry, University of the Basque Country, Leioa 48949, Bizkaia, Spain. E-mail: enrique.hilario@ehu.esDr E Muñoz. Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Hospital Universitario Reina Sofía, Universidad de Córdoba, Córdoba, Spain. e-mail: e.munoz@uco.esDr D Fernández-López. Laboratory of Neonatal Brain Disorders; Department of Neurology UCSF (Parnassus Campus) San Francisco, CA. David.Fernandezlopez@ucsf.edu Dr I Lizasoain. Departamento de Farmacología, Facultad de Medicina, Universidad Complutense, Madrid, Spain. e-mail: ignacio.lizasoain@med.ucm.esDr V Bérézowski. Université Lille Nord de France, Lille, France e-mail: vincent.berezowski@univ-artois.frTarget of this issue:Manuscript Due May 2017First Round of Reviews October 2017Publication DateDecember 2017It is now well established that many of society´s most devastating and costly neurological diseases and disorders arise from trauma at, or shortly after birth. In some cases deficits are seen in childhood and in others they are substantially delayed; arising in adolescence or young adulthood. In either case the initial insult initiates a metabolic and/or neurodegenerative cascade that proceeds, often undetected, for a considerable period of time before diagnosable symptoms appear. Cerebral palsy (CP) describes a group of neurodevelopmental disorders of posture and movement that are frequently associated with sensory, behavioral, and cognitive impairments. The clinical picture of CP has changed with improved neonatal care over the past few decades, resulting in higher survival rates of infants born very preterm. Children born preterm seem particularly vulnerable to perinatal hypoxia-ischemia insults at birth. Most animal models of CP are based on hypoxia-ischemia around the time of birth. In this review, we focus on alterations of brain organization and functions, especially sensorimotor changes, induced by prenatal ischemia in rodents and rabbits, and relate these alterations to neurodevelopmental disorders found in preterm children. We also discuss recent literature that addresses the relationship between neural and myelin plasticity, as well as possible contributions of white matter injury to the emergence of brain dysfunctions induced by prenatal ischemia.