Publications by authors named "Barbara Krauspe"

Widespread inflammatory lesions within the central nervous system grey and white matter are major hallmarks of multiple sclerosis. The development of full-blown demyelinating multiple sclerosis lesions might be preceded by preactive lesions which are characterized by focal microglia activation in close spatial relation to apoptotic oligodendrocytes. In this study, we investigated the expression of signaling molecules of oligodendrocytes that might be involved in initial microglia activation during preactive lesion formation.

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Recently, we proved in the first measurements of breast carcinomas the feasibility of super-resolution ultrasound (US) imaging by motion-model ultrasound localization microscopy in a clinical setup. Nevertheless, pronounced in-plane and out-of-plane motions, a nonoptimized microbubble injection scheme, the lower frame rate and the larger slice thickness made the processing more complex than in preclinical investigations. Here, we compare the results of state-of-the-art contrast-enhanced to super-resolution US imaging and systematically analyze the measurements to get indications for the improvement of image acquisition and processing in the future clinical studies.

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A broad spectrum of diseases is characterized by myelin abnormalities and/or oligodendrocyte pathology. In most, if not all, of these diseases, early activation of microglia occurs. Our knowledge regarding the factors triggering early microglia activation is, however, incomplete.

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Proton magnetic resonance spectroscopy (1H-MRS) is a quantitative MR imaging technique often used to complement conventional MR imaging with specific metabolic information. A key metabolite is the amino acid derivative N-Acetylaspartate (NAA) which is an accepted marker to measure the extent of neurodegeneration in multiple sclerosis (MS) patients. NAA is catabolized by the enzyme aspartoacylase (ASPA) which is predominantly expressed in oligodendrocytes.

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Canavan disease is a spongiform leukodystrophy caused by an autosomal recessive mutation in the aspartoacylase gene. Deficiency of oligodendroglial aspartoacylase activity and a subsequent increase of its substrate N-acetylaspartate are the etiologic factors for the disease. N-acetylaspartate acts as a molecular water pump.

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