scholarly journals New modeling and experimental framework to characterize hindered and restricted water diffusion in brain white matter

2004 ◽  
Vol 52 (5) ◽  
pp. 965-978 ◽  
Author(s):  
Yaniv Assaf ◽  
Raisa Z. Freidlin ◽  
Gustavo K. Rohde ◽  
Peter J. Basser
Keyword(s):  
White Matter ◽  
Water Diffusion ◽  
Brain White Matter ◽  
Diffusion In Brain

scholarly journals Axial asymmetry of water diffusion in brain white matter

2005 ◽  
Vol 54 (4) ◽  
pp. 860-867 ◽  
Author(s):  
Mariana Lazar ◽  
Jong Hoon Lee ◽  
Andrew L. Alexander
Keyword(s):  
White Matter ◽  
Water Diffusion ◽  
Brain White Matter ◽  
Diffusion In Brain

Is water diffusion restricted in human brain white matter? An echo-planar NMR imaging study

Neuroreport ◽  
1993 ◽  
Vol 4 (7) ◽  
pp. 887-890 ◽  
Author(s):  
Denis Le Bihan ◽  
Robert Turner ◽  
Philippe Douek
Keyword(s):  
White Matter ◽  
Human Brain ◽  
Imaging Study ◽  
Water Diffusion ◽  
Nmr Imaging ◽  
Brain White Matter ◽  
Echo Planar

Temperature dependence of water diffusion pools in brain white matter

NeuroImage ◽  
2016 ◽  
Vol 127 ◽  
pp. 135-143 ◽  
Author(s):  
Bibek Dhital ◽  
Christian Labadie ◽  
Frank Stallmach ◽  
Harald E. Möller ◽  
Robert Turner
Keyword(s):  
White Matter ◽  
Temperature Dependence ◽  
Water Diffusion ◽  
Brain White Matter

scholarly journals On the scaling behavior of water diffusion in human brain white matter

NeuroImage ◽  
2019 ◽  
Vol 185 ◽  
pp. 379-387 ◽  
Author(s):  
Jelle Veraart ◽  
Els Fieremans ◽  
Dmitry S. Novikov
Keyword(s):  
White Matter ◽  
Human Brain ◽  
Water Diffusion ◽  
Scaling Behavior ◽  
Brain White Matter

scholarly journals QOL-09. WHOLE-BRAIN WHITE MATTER NETWORK CONNECTIVITY IS DISRUPTED BY PEDIATRIC BRAIN TUMOR TREATMENT

2020 ◽  
Vol 22 (Supplement_3) ◽  
pp. iii432-iii432
Author(s):  
Adeoye Oyefiade ◽  
Kiran Beera ◽  
Iska Moxon-Emre ◽  
Jovanka Skocic ◽  
Ute Bartels ◽  
...  
Keyword(s):  
White Matter ◽  
Pediatric Brain Tumor ◽  
Pediatric Brain Tumors ◽  
Magnetic Resonance Images ◽  
Long Term Effects ◽  
Brain White Matter ◽  
The Right ◽  
Pediatric Brain ◽  
Betweeness Centrality

Abstract INTRODUCTION Treatments for pediatric brain tumors (PBT) are neurotoxic and lead to long-term deficits that are driven by the perturbation of underlying white matter (WM). It is unclear if and how treatment may impair WM connectivity across the entire brain. METHODS Magnetic resonance images from 41 PBT survivors (mean age: 13.19 years, 53% M) and 41 typically developing (TD) children (mean age: 13.32 years, 51% M) were analyzed. Image reconstruction, segmentation, and node parcellation were completed in FreeSurfer. DTI maps and probabilistic streamline generation were completed in MRtrix3. Connectivity matrices were based on the number of streamlines connecting two nodes and the mean DTI (FA) index across streamlines. We used graph theoretical analyses to define structural differences between groups, and random forest (RF) analyses to identify hubs that reliably classify PBT and TD children. RESULTS For survivors treated with radiation, betweeness centrality was greater in the left insular (p < 0.000) but smaller in the right pallidum (p < 0.05). For survivors treated without radiation (surgery-only), betweeness centrality was smaller in the right interparietal sulcus (p < 0.05). RF analyses showed that differences in WM connectivity from the right pallidum to other parts of the brain reliably classified PBT survivors from TD children (classification accuracy = 77%). CONCLUSIONS The left insular, right pallidum, and right inter-parietal sulcus are structurally perturbed hubs in PBT survivors. WM connectivity from the right pallidum is vulnerable to the long-term effects of treatment for PBT.

scholarly journals Pioglitazone Ameliorates Lipopolysaccharide-Induced Behavioral Impairment, Brain Inflammation, White Matter Injury and Mitochondrial Dysfunction in Neonatal Rats

2021 ◽  
Vol 22 (12) ◽  
pp. 6306
Author(s):  
Jiann-Horng Yeh ◽  
Kuo-Ching Wang ◽  
Asuka Kaizaki ◽  
Jonathan W. Lee ◽  
Han-Chi Wei ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
White Matter ◽  
Brain Inflammation ◽  
White Matter Injury ◽  
Neonatal Rat ◽  
Mitochondrial Activity ◽  
Neonatal Rats ◽  
Activated Microglia ◽  
Brain White Matter ◽  
Performance Reduction

Previous studies have demonstrated that pioglitazone, a peroxisome proliferator-activated receptor gamma (PPARγ) agonist, inhibits ischemia-induced brain injury. The present study was conducted to examine whether pioglitazone can reduce impairment of behavioral deficits mediated by inflammatory-induced brain white matter injury in neonatal rats. Intraperitoneal (i.p.) injection of lipopolysaccharide (LPS, 2 mg/kg) was administered to Sprague–Dawley rat pups on postnatal day 5 (P5), and i.p. administration of pioglitazone (20 mg/kg) or vehicle was performed 5 min after LPS injection. Sensorimotor behavioral tests were performed 24 h after LPS exposure, and changes in biochemistry of the brain was examined after these tests. The results show that systemic LPS exposure resulted in impaired sensorimotor behavioral performance, reduction of oligodendrocytes and mitochondrial activity, and increases in lipid peroxidation and brain inflammation, as indicated by the increment of interleukin-1β (IL-1β) levels and number of activated microglia in the neonatal rat brain. Pioglitazone treatment significantly improved LPS-induced neurobehavioral and physiological disturbances including the loss of body weight, hypothermia, righting reflex, wire-hanging maneuver, negative geotaxis, and hind-limb suspension in neonatal rats. The neuroprotective effect of pioglitazone against the loss of oligodendrocytes and mitochondrial activity was associated with attenuation of LPS-induced increment of thiobarbituric acid reactive substances (TBARS) content, IL-1β levels and number of activated microglia in neonatal rats. Our results show that pioglitazone prevents neurobehavioral disturbances induced by systemic LPS exposure in neonatal rats, and its neuroprotective effects are associated with its impact on microglial activation, IL-1β induction, lipid peroxidation, oligodendrocyte production and mitochondrial activity.

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