scholarly journals Oligodendrocyte Development and Implication in Perinatal White Matter Injury

2021 ◽  
Vol 15 ◽  
Author(s):  
Mahsa Motavaf ◽  
Xianhua Piao
Keyword(s):  
White Matter ◽  
Therapeutic Strategy ◽  
Treatment Options ◽  
Unmet Need ◽  
Functional Restoration ◽  
White Matter Injury ◽  
Neurological Deficits ◽  
Oligodendrocyte Development ◽  
Underlying Pathophysiology ◽  
Ischemic Events

Perinatal white matter injury (WMI) is the most common brain injury in premature infants and can lead to life-long neurological deficits such as cerebral palsy. Preterm birth is typically accompanied by inflammation and hypoxic-ischemic events. Such perinatal insults negatively impact maturation of oligodendrocytes (OLs) and cause myelination failure. At present, no treatment options are clinically available to prevent or cure WMI. Given that arrested OL maturation plays a central role in the etiology of perinatal WMI, an increased interest has emerged regarding the functional restoration of these cells as potential therapeutic strategy. Cell transplantation and promoting endogenous oligodendrocyte function are two potential options to address this major unmet need. In this review, we highlight the underlying pathophysiology of WMI with a specific focus on OL biology and their implication for the development of new therapeutic targets.

scholarly journals White matter injury induced by diabetes in acute stroke is clinically relevant: A preliminary study

2016 ◽  
Vol 14 (1) ◽  
pp. 40-46 ◽  
Author(s):  
Xinfeng Yu ◽  
Ruirui Song ◽  
Yerfan Jiaerken ◽  
Lixia Yuan ◽  
Peiyu Huang ◽  
...  
Keyword(s):  
White Matter ◽  
Fractional Anisotropy ◽  
Corticospinal Tract ◽  
Diffusion Tensor ◽  
White Matter Injury ◽  
Neurological Deficits ◽  
Diabetic Patients ◽  
Stroke Severity ◽  
Superior Longitudinal Fasciculus ◽  
Poor Outcome

The importance of white matter injury induced by diabetes in stroke severity and prognosis is largely unknown. We aimed to investigate the relationship between diabetes-related white matter injury beyond stroke lesions with acute neurological deficits and clinical outcome after stroke. In total, 36 stroke patients within 3–7 days after onset were enrolled. Neurological deficits on admission were assessed by National Institute of Health Stroke Score, and poor outcome at 3 months was defined as modified Rankin score >2. White matter tracts were compared between patients with diabetic and non-diabetic stroke using fractional anisotropy from diffusion tensor imaging. Regional white matter abnormality with decreased fractional anisotropy was observed in diabetic patients ( n = 18) when compared to non-diabetic patients ( n = 18). Decreased fractional anisotropy in ipsilesional distal corticospinal tract was independently associated with higher National Institute of Health Stroke Score motor component score ( β = −0.444, p = 0.005), and decreased fractional anisotropy in contralesional superior longitudinal fasciculus I was independently related to poor outcome (odds ratio, 0.900; p = 0.033). Our findings suggested that only white matter injury induced by diabetes in specific tracts like corticospinal tract and superior longitudinal fasciculus beyond stroke lesions has clinically relevant, providing insight into the mechanism of stroke recovery under the diabetic condition.

Clobetasol Attenuates White Matter Injury by Promoting Oligodendrocyte Precursor Cell Differentiation

2020 ◽  
Vol 55 (4) ◽  
pp. 188-196
Author(s):  
Xuewen Su ◽  
Haifeng Yuan ◽  
Yuxin Bai ◽  
Junlong Chen ◽  
Mingze Sui ◽  
...  
Keyword(s):  
White Matter ◽  
Rat Model ◽  
Myelin Sheath ◽  
White Matter Injury ◽  
Neurological Deficits ◽  
Treatment Groups ◽  
Myelin Sheaths ◽  
Neurobehavioral Function ◽  
Sheath Formation ◽  
Oligodendrocyte Precursor

<b><i>Introduction:</i></b> White matter injury (WMI) is the most common brain injury in preterm infants and can result in life-long neurological deficits. The main cause of WMI is damage to the oligodendrocyte precursor cells (OPC) in the brain that results in delayed myelin sheath formation, or the destruction of existing myelin sheaths. OPC undergo highly regulated and strictly timed developmental changes that result in their transformation to mature oligodendrocytes capable of myelin production. <b><i>Objective:</i></b> Studies have shown that clobetasol strongly promotes differentiation of OPC into myelin sheaths. Therefore, we hypothesized that clobetasol may be a therapeutic option for the treatment of preterm WMI. <b><i>Methods:</i></b> We induced a WMI rat model and observed white matter damage under an optical microscope. Rats subjected to WMI were injected intraperitoneally with clobetasol (2 or 5 mg/kg daily) from day 1 to day 5 in the early treatment groups, or from day 6 to day 10 in the late treatment groups. After 17 days, the rats were sacrificed and the expression of myelin basic protein (MBP) was visualized using immunofluorescence. In addition, we evaluated myelin sheath formation using electron microscopy. The rats were also subjected to the suspension test, ramp test, and open field test to evaluate neurobehavioral functions. <b><i>Results:</i></b> A rat model of WMI was successfully induced. It was found that clobetasol significantly induced MBP expression and myelin sheath formation and improved neurobehavioral function in the rats subjected to WMI. <b><i>Conclusions:</i></b> Our results indicate that clobetasol attenuates WMI by promoting OPC differentiation, and it may be an effective therapeutic agent for the treatment of preterm WMI.

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