Humboldt Research Fellow, Neurologische Klinik, Klinikum Grosshadern, Marchioninstrasse 15, 81377 München, Germany.
Practical Neurology 03/2008; 8(1):26-38. DOI: 10.1136/jnnp.2007.139428
Source: PubMed


Leukoaraiosis describes diffuse white matter abnormalities on CT or MR brain scans, often seen in the normal elderly and in association with vascular risk factors such as hypertension, or in the context of cognitive impairment. The term was introduced to avoid confusing an imaging appearance with a specific pathology. Neurologists often come across this appearance, but its significance is sometimes uncertain. The effects on cognitive function and gait are insidious and can be difficult to detect at the bedside, but are nevertheless important. However, gradually it is becoming clearer how leukoaraiosis relates to cerebrovascular disease, Alzheimer's and other diseases, and how this appearance should influence treatment decisions.

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    • "These findings support our hypothesis that SphK1−/− animals are more susceptible to the injury and that deletion of it affects the baseline response to LPS. Leukoaraiosis is a loss of white matter that is usually associated with vascular risk factors such as hypertension, or in the context of cognitive impairment [38]. On the other hand, there are several reports where leukoaraiosis was found to be in a close relationship with the inflammatory markers [39] and loss of oligodendrocytes, followed by demyelination [40]. "
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    ABSTRACT: The pathogenesis of inflammation in the central nervous system (CNS), which contributes to numerous neurodegenerative diseases and results in encephalopathy and neuroinflammation, is poorly understood. Sphingolipid metabolism plays a crucial role in maintaining cellular processes in the CNS, and thus mediates the various pathological consequences of inflammation. For a better understanding of the role of sphingosine kinase activation during neuroinflammation, we developed a bacterial lipopolysaccharide (LPS)-induced brain injury model. The onset of the inflammatory response was observed beginning 4 hours after intracerebral injection of LPS into the lateral ventricles of the brain. A comparison of established neuroinflammatory parameters such as white matter rarefactions, development of cytotoxic edema, astrogliosis, loss of oligodendrocytes, and major cytokines levels in wild type and knockout mice suggested that the neuroinflammatory response in SphK1−/− mice was significantly upregulated. At 6 hours after intracerebroventricular injection of LPS in SphK1−/− mice, the immunoreactivity of the microglia markers and astrocyte marker glial fibrillary acidic protein (GFAP) were significantly increased, while the oligodendrocyte marker O4 was decreased compared to WT mice. Furthermore, western blotting data showed increased levels of GFAP. These results suggest that SphK1 activation is involved in the regulation of LPS induced brain injury. Research Highlights • Lipopolysaccharide (LPS) intracerebral injection induces severe neuroinflammation. • Sphingosine kinase 1 deletion worsens the effect of the LPS. • Overexpression of SphK1 might be a potential new treatment approach to neuroinflammation.
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