Literature DB >> 15017012

Positron emission tomography examination of cerebral blood flow and glucose metabolism in young CADASIL patients.

Susanna Tuominen1, Qing Miao, Timo Kurki, Seppo Tuisku, Minna Pöyhönen, Hannu Kalimo, Matti Viitanen, Hannu T Sipilä, Jörgen Bergman, Juha O Rinne.   

Abstract

BACKGROUND AND
PURPOSE: CADASIL causes repeated ischemic strokes leading to subcortical vascular dementia. The purpose of this study was to assess whether cerebral blood flow (CBF) and regional cerebral metabolic rates of glucose (rCMR(gluc)) in CADASIL patients are affected in early adulthood.
METHODS: CBF and rCMR(gluc) were examined with positron emission tomography in correlation with magnetic resonance imaging (MRI) in 14 adult (19 to 41 years) CADASIL patients with the Notch3 R133C mutation. Seven patients had experienced transient ischemic attack and 3 had experienced > or =1 strokes.
RESULTS: The mean CBF in the CADASIL patients was significantly lower in both frontal (P=0.019) and occipital (P=0.009) white matter (WM) than those in the controls. CBF decreased significantly with increased severity of the disease. The patients had lower mean rCMR(gluc) values than the controls, although differences were not statistically significant. Sum scores of semiquantitative MRI rating scale (Scheltens) correlated significantly with WM CBF but not with rCMR(gluc).
CONCLUSIONS: In CADASIL, there is an early and significant decrease in the CBF of WM associated with simultaneous MRI changes. These are obviously caused by the arteriopathy in long penetrating arteries and indicate early tissue damage, also expressed as impaired rCMR(gluc) in the WM.

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Year:  2004        PMID: 15017012     DOI: 10.1161/01.STR.0000124124.69842.2d

Source DB:  PubMed          Journal:  Stroke        ISSN: 0039-2499            Impact factor:   7.914


  24 in total

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Review 3.  CADASIL: experimental insights from animal models.

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Journal:  Stroke       Date:  2010-10       Impact factor: 7.914

Review 4.  CADASIL: Treatment and Management Options.

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5.  CADASIL mutant NOTCH3(R90C) decreases the viability of HS683 oligodendrocytes via apoptosis.

Authors:  Mibo Tang; Changhe Shi; Bo Song; Jing Yang; Ting Yang; Chengyuan Mao; Yusheng Li; Xinjing Liu; Shuyu Zhang; Hui Wang; Haiyang Luo; Yuming Xu
Journal:  Mol Biol Rep       Date:  2017-06-10       Impact factor: 2.316

6.  Novel pathological features and potential therapeutic approaches for CADASIL: insights obtained from a mouse model of CADASIL.

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Review 7.  Smooth muscle cell phenotypic switching in stroke.

Authors:  Marine Poittevin; Pierre Lozeron; Rose Hilal; Bernard I Levy; Tatiana Merkulova-Rainon; Nathalie Kubis
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8.  Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy: a genetic cause of cerebral small vessel disease.

Authors:  Jay Chol Choi
Journal:  J Clin Neurol       Date:  2010-03-26       Impact factor: 3.077

9.  Neuropathological correlates of temporal pole white matter hyperintensities in CADASIL.

Authors:  Yumi Yamamoto; Masafumi Ihara; Carina Tham; Roger W C Low; Janet Y Slade; Tim Moss; Arthur E Oakley; Tuomo Polvikoski; Raj N Kalaria
Journal:  Stroke       Date:  2009-04-09       Impact factor: 7.914

10.  Interleaved imaging of cerebral hemodynamics and blood flow index to monitor ischemic stroke and treatment in rat by volumetric diffuse optical tomography.

Authors:  Zi-Jing Lin; Ming Ren; Lin Li; Yueming Liu; Jianzhong Su; Shao-Hua Yang; Hanli Liu
Journal:  Neuroimage       Date:  2013-07-16       Impact factor: 6.556

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