Noam Shemesh

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Li Liu¹, Ryan Hunt¹, Hari Rallapalli¹, Nikorn Pothayee¹, Stephen Dodd¹, Nadia Bouraoud¹, Dragan Maric¹, Gary Zabow², and Alan P Koretsky^1
1National Institute of Neurological Disorders and Stroke, National Institute of Health, Bethesda, MD, United States, ²Magnetic Imaging Group, National Institute of Standards and Technology, Boulder, CO, United States

Keywords: Neuroinflammation, Neuroinflammation

High fat diet (HFD) causes chronic low-grade inflammation and is associated with an increased risk of cerebrovascular pathology and neurodegenerative disorders. Hypothalamus can sense peripheral signals and has been the major focus of HFD induced neuroinflammation. This work aims to study the activation of BBB endothelial cells, immune cell infiltration, and brain cell inflammation in the whole brain in real time caused by short-term HFD. Molecular MRI, using a new ultrahigh moment microfabricated gold-iron micro-disc, provides non-invasive guidance to the histology study.  Our data indicate that HFD causes neuroinflammation in a remarkably short time in many structures of brain.

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Do-Wan Lee¹, Jae-Im Kwon², Hwon Heo³, Chul‐Woong Woo⁴, Yeon Ji Chae³, Na Hee Yu², Seongwon Na⁵, Yousun Ko¹, Nari Kim⁶, Joongkee Min⁴, Monica Young Choi⁴, Kyung Won Kim¹, and Dong‐Cheol Woo^3,4
1Department of Radiology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea, Republic of, ²QuBEST Bio Co. ltd., Gyeonggi-do, Korea, Republic of, ³Department of Convergence Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea, Republic of, ⁴Convergence Medicine Research Center, Asan Institute for Life Sciences, Asan Medical Center, Seoul, Korea, Republic of, ⁵Biomedical Research Center, Asan Institute for Life Sciences, Asan Medical Center, Seoul, Korea, Republic of, ⁶Department of Medical Science, Asan Medical Institute of Convergence Science and Technology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea, Republic of

Keywords: Neuroinflammation, Molecular Imaging

Glutamate-weighted chemical exchange saturation transfer (GluCEST) is a useful imaging tool which is used to detect glutamate signal alterations caused by neuroinflammation. The present study quantitatively evaluated glutamate level changes in the hippocampal region of a rat model of sepsis-induced brain injury using GluCEST and proton magnetic resonance spectroscopy (1H-MRS). The GluCEST and 1H-MRS results showed that GluCEST values and glutamate concentrations were significantly higher in the sepsis-induced rats than in the controls. GluCEST imaging could be a helpful technique for defining a biomarker to estimate the glutamate-related metabolism in sepsis-associated diseases.

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Keywords: Multiple Sclerosis, Brain

Inflammation is a pathological characteristic of multiple sclerosis (MS). Individuals with MS are reported to experience reductions in cerebral blood flow (CBF) and brain hypoxia (low oxygenation). The cause of these phenomena is not well-known. We studied the possible association between inflammation and hypoxia in an inflammatory mouse model by quantifying CBF (arterial-spin labeling MRI) and magnetic susceptibility (quantitative susceptibility mapping), as well as measuring hippocampal oxygen using oxygen-sensitive probes. We found that inflammation is associated with reductions in CBF, brain susceptibility, and hippocampal oxygenation. This supports the idea that inflammation can induce brain hypoxia and disrupt cerebrovascular autoregulation.

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Zilin Chen¹, Jianpan Huang¹, Haoyun Su^1,2, Wai Po Chong³, and Kannie W.Y. Chan^1,2,4,5,6
1Department of Biomedical Engineering, City University of Hong Kong, Hong Kong, China, ²Hong Kong Centre for Cerebro-Cardiovascular Health Engineering (COCHE), Hong Kong, China, ³School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China, ⁴Russell H. Morgan Department of Radiology and Radiological Science, The Johns Hopkins University School of Medicine, Baltimore, MD, United States, ⁵City University of Hong Kong Shenzhen Research Institute, Shenzhen, China, ⁶Tung Biomedical Science Centre, City University of Hong Kong, Hong Kong, China

Keywords: Alzheimer's Disease, Neuroscience

Immune cell activation is a hallmark of Alzheimer’s disease (AD). Microglia activation impairs with glucose metabolism, which may serve as early biomarker for AD. Here, we employed dynamic glucose-enhanced (DGE)-MRI to assess glucose uptake and clearance in AD, and study its relationship with microglia based on our previous study. We observed an increase in microglia in AD than WT, accompanied with relatively high parenchymal glucose uptake and low CSF clearance. We believe further studies to associate the underlying molecular and cellular pathology of AD with DGE-MRI could benefit the identification of AD in early stages.

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Keywords: Stroke, Inflammation

Diffusion tensor imaging (DTI) and neurite orientation and density imaging (NODDI) is used to observe regional changes in brain microstructure following intracerebral haemorrhage (ICH) in rats. On day 7 following ICH, DTI and NODDI metrics were significantly altered in haemorrhaged sub-regions as well as healthy appearing overlying cortex, compared to contralateral tissue. Histological analysis suggest these changes are driven by altered cell density and populations, with notable regional changes in microglia/macrophages. In summary, DTI and NODDI parameters are altered in ICH and may reflect changes in the immune cell populations in both haemorrhaged and overlying normal-appearing cortex.  

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Jonas Yeung^1,2, Taylor De Young¹, Shoshana Spring¹, Qi Xiao³, Jason Lerch⁴, Mark Palmert⁵, and Brian J. Nieman^1,2,6
1Translational Medicine, The Hospital for Sick Children, Toronto, ON, Canada, ²Medical Biophysics, University of Toronto, Toronto, ON, Canada, ³The Hospital for Sick Children, Toronto, ON, Canada, ⁴Wellcome Centre for Integrative Neuroimaging, University of Oxford, Oxford, United Kingdom, ⁵Department of Paediatrics, The Hospital for Sick Children, Toronto, ON, Canada, ⁶Ontario Institute for Cancer Research, Toronto, ON, Canada

Keywords: Neuroinflammation, Preclinical, mouse, structural, radiation, Ccl2

Females tend to exhibit worse cognitive outcomes than males after pediatric cranial radiation therapy (CRT). Previous literature suggest that these sex differences may be driven by neuroinflammatory responses that involve CCL2. The objective of this study was to determine whether protection from Ccl2 knockout is mediated by sex hormones or sex chromosomes. We employ MRI on a CRT mouse model with mixed sex hormone and chromosome complements (i.e., four core genotypes model) to determine neuroanatomical changes. We found that both male chromosome and male sex hormones separately benefit regions of the brain in CCL2 deficient mice after CRT.

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Keywords: Brain Connectivity, fMRI (resting state), Light sedation

Post traumatic brain injury (TBI) neuroinflammation has been linked to many long-term outcomes of TBI. To better understand the interrelationship of the neuroinflammation and changes of functional connectivity, we followed rats after TBI in a series of functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) experiments. We observed hypoconnectivity in the corticothalamic connections, which was laterally altered at the acute time point and correlated with the observed level of neuroinflammation in the lateroposterior thalamic nuclei. This sheds light on the potential role of focal post-traumatic neuroinflammation shaping large scale functional connectivity in the post-traumatic brain.

Xuhong Yang¹, Pei Dang², Jiarui Zheng¹, Min Li³, Ruirui Lv¹, and Xiaodong Wang^2
1Ningxia Medical University, Yingchuan, China, ²Department of Radiology, General Hospital of Ningxia Medical University, Yingchuan, China, ³GE Healthcare, MR Enhancement Application, Beijing, China

Keywords: Neurodegeneration, Quantitative Susceptibility mapping, Minimal hepatic encephalopathy; Iron

In this study, we used the QSM technique to quantitatively evaluate the levels of brain iron in the hippocampus of MHE rats and by evaluating the neuroinflammatory response to explore the relationship between iron with neuroinflammation and cognition. It is expected to provide important insights into the occurrence of MHE disease symptoms and the related biological mechanisms behind them. Meanwhile, our findings also suggested that an abnormal susceptibility values in certain brain areas identified using the QSM may be a potential biomarker to reflect the severity of cognitive impairment and to monitor its progression in cirrhotic patients with MHE.

Rania Muhammed¹, Rehman Tariq ², Uche J Ohaezukosi², Qandeel Shafqat², Ying Wu², and Jeff F. Dunn^1
1University of Calgary, Calgary, AB, Canada, ²Department of Radiology, University of Calgary, Calgary, AB, Canada

Keywords: Multiple Sclerosis, Brain

Multiple sclerosis is an inflammatory disease of the central nervous system, with a posited hypoxia-inflammation cycle hypothesis. Hypoxia may increase disease severity in MS. We found R2* was increased (an MRI marker of hypoxia) in the cortex. We observed increased sickness and R2* in EAE mice compared to controls, but reduced CBF in both CFA-PTx and EAE.  Inflammation is in both groups, while autoimmunity is only in EAE. Reduced CBF may relate to inflammation, whereas hypoxia may relate to autoimmune-mediated damage and increase disease severity. 

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Martin Kozár^1,2, Laura Parkes^1,2, Hervé Boutin³, Igor Chernyavsky⁴, and Ben Dickie^2,5
1Division of Psychology, Communication and Human Neuroscience, School of Health Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, United Kingdom, ²Geoffrey Jefferson Brain Research Centre, Manchester Academic Health Science Centre, Manchester, United Kingdom, ³Division of Neuroscience, School of Biological Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, United Kingdom, ⁴Department of Mathematics, The University of Manchester, Manchester, United Kingdom, ⁵Division of Informatics, Imaging and Data Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, United Kingdom

Keywords: Neurofluids, Alzheimer's Disease, Perivascular space

Enlargement of perivascular and ventricular spaces are associated with neuroinflammation in neurodegenerative diseases, including cerebral small vessel disease and Alzheimer’s disease. In this study we develop methodology for measuring the anatomy of the perivascular space around the anterior cerebral artery and partial-volume-free estimates of total CSF volume and apply this approach to TgF344-AD rats. Neither the area under the curve of perivascular space profiles, nor overall width of the perivascular space, or the total CSF volume differed between TgF344-AD rats and wild-types.