Journal of neuroimaging : official journal of the American Society of Neuroimaging
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Imaging transcriptomics investigates the relationship between neuroanatomical/neuroimaging features and gene expression. The spatial and temporal distribution of the expressed genes and their pattern of spreading over time can contribute to elucidating cellular and molecular processes involved in neurodegeneration. In this study, we review recent findings regarding the correlation between neuroimaging and expression data in neurodegenerative diseases with a focus on Alzheimer's disease and Parkinson's disease. ⋯ In addition, expression enrichment of genes involved in immunological processes in vulnerable regions-such as the Toll-like receptor, a receptor involved in innate immunity-plays a major role in neuroinflammation in neurodegenerative diseases. However, substantial limitations must be overcome in future studies: the lack of high-quality resolution expression data, the lack of standardized study protocols, and insufficient sensitive early stage neuroimaging markers of degeneration. Identifying neuroimaging and expression prodromal biomarkers and investigating their causal relation in the preclinical disease stage may enable early targeted therapy before the onset of irreversible brain changes.
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Gait impairment is a hallmark of Parkinson's disease (PD). Natural walking involves more cognitive demand than treadmill walking or in-laboratory walking tests because patients have to actively work on navigation and top-down cognitive control which taxes cognitive reserve in the prefrontal cortex. To mimic the prefrontal engagement occurring with natural walking in a controlled and safe environment, dual-task (DT) treadmill walking has been developed. In this study, we tested the feasibility of imaging DT walking-related changes in brain glucose metabolism in patients with PD. ⋯ This study confirms the feasibility of imaging glucose metabolism during DT walking in patients with PD. We also report that during DT walking, there is a lesser degree of prefrontal engagement in the patients with more progressed disease compared to those with less progressed disease, implying increased degrees of frontal dysfunction with PD progression.
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For diagnosis of medulloblastoma, the updated World Health Organization classification now demands for genetic typing, defining more precisely the tumor biology, therapy, and prognosis. We investigated potential associations between magnetic resonance imaging (MRI) parameters including apparent diffusion coefficient (ADC) and neuropathologic features of medulloblastoma, focusing on genetic subtypes. ⋯ MRI analysis enabled noninvasive differentiation of SHH-activated medulloblastoma. ADC alone was not reliable for genetic characterization, but associated with tumor proliferation rate.
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Observational Study
Multimodal MRI Response to Fingolimod in Multiple Sclerosis: A Nonrandomized, Single Arm, Observational Study.
Fingolimod has a favorable effect on conventional MRI measures; however, its neuroprotective effect is not clear. We aim to investigate changes of conventional and advanced MRI measures in lesions and normal-appearing white matter (NAWM) over 2 years in fingolimod-treated patients. ⋯ These findings suggest a possible neuroreparative effect of fingolimod on the MS lesions and NAWM. Larger and longer randomized studies are required to confirm these results.
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Cervical carotid artery (cCA) dolichoectasia (DE) is characterized by elongation, tortuosity, and/or dilatation. The prevalence of cCA DE has been reported 13-31% in population-based and 14-58% in hospital-based studies. The exact mechanisms of this aberrant arterial remodeling are unknown. ⋯ Prospectively, people with cCA DE have a higher risk of vascular events, although it is uncertain if the risk of stroke is also higher in this population. In the absence of alternative stroke etiologies, stroke patients with cCA DE should be considered to have had a cryptogenic stroke and treated with daily antiplatelet therapy. Further population-based studies are needed to clarify whether specific therapies may be implement to reduce the risk of events among people with cCA DE.