» Articles » PMID: 22363841

Molecular Mechanisms of Neonatal Brain Injury

Overview
Journal Neurol Res Int
Publisher Wiley
Specialty Neurology
Date 2012 Feb 25
PMID 22363841
Citations 65
Authors
Affiliations
Soon will be listed here.
Abstract

Fetal/neonatal brain injury is an important cause of neurological disability. Hypoxia-ischemia and excitotoxicity are considered important insults, and, in spite of their acute nature, brain injury develops over a protracted time period during the primary, secondary, and tertiary phases. The concept that most of the injury develops with a delay after the insult makes it possible to provide effective neuroprotective treatment after the insult. Indeed, hypothermia applied within 6 hours after birth in neonatal encephalopathy reduces neurological disability in clinical trials. In order to develop the next generation of treatment, we need to know more about the pathophysiological mechanism during the secondary and tertiary phases of injury. We review some of the critical molecular events related to mitochondrial dysfunction and apoptosis during the secondary phase and report some recent evidence that intervention may be feasible also days-weeks after the insult.

Citing Articles

Methadone directly impairs central nervous system cells in vitro.

De Gregorio C, Gallardo J, Berrios-Carcamo P, Handy A, Santapau D, Gonzalez-Madrid A Sci Rep. 2024; 14(1):16978.

PMID: 39043899 PMC: 11266518. DOI: 10.1038/s41598-024-67860-7.


Leflunomide Treatment Does Not Protect Neural Cells following Oxygen-Glucose Deprivation (OGD) In Vitro.

Curel C, Nobeli I, Thornton C Cells. 2024; 13(7.

PMID: 38607070 PMC: 11011260. DOI: 10.3390/cells13070631.


Neuroprotective Action of Tacrolimus before and after Onset of Neonatal Hypoxic-Ischaemic Brain Injury in Rats.

Smith M, Penny T, Pham Y, Sutherland A, Jenkin G, Fahey M Cells. 2023; 12(22).

PMID: 37998394 PMC: 10669941. DOI: 10.3390/cells12222659.


Protein Carbonylation as a Biomarker of Oxidative Stress and a Therapeutic Target in Neonatal Brain Damage.

Martinez-Orgado J, Martinez-Vega M, Silva L, Romero A, de Hoz-Rivera M, Villa M Antioxidants (Basel). 2023; 12(10).

PMID: 37891918 PMC: 10603858. DOI: 10.3390/antiox12101839.


[Biomarkers and neuromonitoring for prognosis of development after perinatal brain damage].

Felderhoff-Muser U, Huning B Monatsschr Kinderheilkd. 2022; 170(8):688-703.

PMID: 35909417 PMC: 9309449. DOI: 10.1007/s00112-022-01542-4.


References
1.
Woods A, Dickerson K, Heath R, Hong S, Momcilovic M, Johnstone S . Ca2+/calmodulin-dependent protein kinase kinase-beta acts upstream of AMP-activated protein kinase in mammalian cells. Cell Metab. 2005; 2(1):21-33. DOI: 10.1016/j.cmet.2005.06.005. View

2.
Lorek A, Takei Y, Cady E, Wyatt J, Penrice J, Edwards A . Delayed ("secondary") cerebral energy failure after acute hypoxia-ischemia in the newborn piglet: continuous 48-hour studies by phosphorus magnetic resonance spectroscopy. Pediatr Res. 1994; 36(6):699-706. DOI: 10.1203/00006450-199412000-00003. View

3.
van der Kooij M, Nijboer C, Ohl F, Groenendaal F, Heijnen C, van Bel F . NF-kappaB inhibition after neonatal cerebral hypoxia-ischemia improves long-term motor and cognitive outcome in rats. Neurobiol Dis. 2010; 38(2):266-72. DOI: 10.1016/j.nbd.2010.01.016. View

4.
Dirnagl U, Iadecola C, Moskowitz M . Pathobiology of ischaemic stroke: an integrated view. Trends Neurosci. 1999; 22(9):391-7. DOI: 10.1016/s0166-2236(99)01401-0. View

5.
Cassidy-Stone A, Chipuk J, Ingerman E, Song C, Yoo C, Kuwana T . Chemical inhibition of the mitochondrial division dynamin reveals its role in Bax/Bak-dependent mitochondrial outer membrane permeabilization. Dev Cell. 2008; 14(2):193-204. PMC: 2267902. DOI: 10.1016/j.devcel.2007.11.019. View