Abstract DZNE-2020-01027

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Characterization of cerebral small vessel disease in SHRSP: A longitudinal MRI study at 3.0 Tesla

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2013

European Stroke Conference, LondonLondon, UK, 28 May 2013 - 31 May 20132013-05-282013-05-31

Abstract: Background:Human cerebral small vessel disease (CSVD, cerebral microangiopathy) is one of the leading causes of vascular dementia and ischemic stroke and is caused by degenerative small vessel wall chang-es. In spontaneously hype1tensive stroke-prone rats (SHRSP), a wen-established animal model of.SVD, we recently showed that cerebral microangiopathy develops in distinct histopathologicall teps initiated by intracapillary and -arteriolar erythrocyte accumulations. This early microvascular dysfunction is followed by blood brain banier (BBB) disruption, subsequent Inicrobleeds and final­ ly hemorrhagic infarcts and intraparenchymal hermon-hage.In the present study we aimed to vetify this pathophysiological cascade non-invasively by serial magnetic resonance imaging (MRI). Methods:Fourteen SHRSP and three control rats (Wistar) aged between 26 and 42 weeks were repeatedly investigated by 3.0 Tesla MRI (Siemens Trio) including Tl-weighted, T2-weighted, T2 CISS 3D, FLAIR and GRE images. Animals were perfused for H&E staining at (i) an age of 42 weeks or (ii) after developing stroke-like symptoms or (iii) as soon as MRI revealed pathologies including hyper­ or hypointensities. Histology was conelated with the MRI dataResults:Terininal stages of the CSVD cascade. including larger intraparenchymal hemmThages and infarcts could be consistently detected by MRI and were confirmed histologically. However, 3.0 Tesla MRl failed to visualize Inicrobleeds (< 150 mm) which were frequently found in histology. Moreover, there was no MRl correlate of the initialtnicrovascular dysfunction including llllllinal erythrocyte accumulations in small brain vessels.Conclusion:MRI at field strength of 3.0 Tesla can only partially depict the pathological changes in the brains of SHRSP. Further investigations at higher magnetic field strengths (7.0 Tesla) using blood- and flow-sensitive sequences are cunently underway to increase the diagnostic sensitivity.


Contributing Institute(s):
  1. Pathophysiology of Dementia (AG Reymann)
Research Program(s):
  1. 342 - Disease Mechanisms and Model Systems (POF3-342) (POF3-342)

Appears in the scientific report 2013
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Institute Collections > MD DZNE > MD DZNE-AG Reymann
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 Record created 2020-08-26, last modified 2020-09-25


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