Christian Zammit¹ and Mario Valentino²*

¹Department of Anatomy, University of Malta, Msida, Malta
²Department of Physiology and Biochemistry, University of Malta, Msida, Malta

*Corresponding Author: Mario Valentino, Department of Physiology and Biochemistry, University of Malta, Msida, Malta.

Received: May 23,2022; Published:

Abstract

Preterm cerebral white matter injury (WMI) frequently encompasses hypoxic–ischemic lesions such as periventricular leukomalacia (PVL) and hypoxic–ischemic encephalopathy (HIE). These infants are extremely vulnerable to brain injury and are at high risk of developing motor and cognitive abnormalities at later stages in life.

Although preoligodendrocytes (preOLs) have long been regarded as the hallmark of perinatal white matter injury [1], we have previously reported that late pre-myelinating axons having initiated diameter expansion and expressing clusters of functional voltage-gated calcium channels, are equally principal targets for injury during heightened periods of selective vulnerability to hypoxia-ischemia.  By contrast, axons yet to enter this developmental window, or which have already initiated myelination, have a much higher ischemic tolerance [2]. The burden of WMI in a given region is thus likely to be influenced by the complement of late pre-myelinating axons and preOLs in the affected white matter structures. These findings suggest that damage to developing axons is a major, but previously underappreciated component of perinatal WMI and which as to date remains without any cure [2].

References

1. Back SA., et al. “Selective vulnerability of late oligodendrocyte progenitors to hypoxia-ischemia”. Journal of Neuroscience 2 (2002): 455-463.
2. Alix JJ., et al. “Central axons preparing to myelinate are highly sensitive to ischaemic injury”. Annals of Neurology 6 (2012): 936-951.
3. JR Buser., et al. “Arrested preoligodendrocyte maturation contributes to myelination failure in premature infants”. Annals of Neurology 71 (2012): 93-109.
4. Segovia KN., et al. “Arrested oligodendrocyte lineage maturation in chronic perinatal white matter injury”. Annals of Neurology 63 (2008): 520-530.
5. JM Dean., et al. “What brakes the preterm brain? An arresting story”. Pediatric Research 75 (2014): 227-233.
6. SA Back and SP Miller. “Brain injury in premature neonates: A primary cerebral dysmaturation disorder?” Annals of Neurology 75(2014): 469-486.
7. Z Molnar and M Rutherford. “Brain maturation after preterm birth”. Science Translational Medicine 5 (2013): 168ps2.
8. Fields RD. “White matter in learning, cognition and psychiatric disorders”. Trends in Neurosciences 31 (2008): 361-370.
9. Schrager P and Novakovic SD. “Control of myelination, axonal growth, and synapse formation in spinal cord explants by ion channels and electrical activity”. Brain Research Developmental Brain Research 88 (1995): 68-78.

Citation

Citation: Christian Zammit and Mario Valentino. “The Link between Cognitive Deficits and White Matter Injury in Preterms". Acta Scientific Neurology 5.7 (2022): 21-22.

Copyright

Copyright: © 2022 Christian Zammit and Mario Valentino. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.