Large scale research studies combining magnetic resonance imaging data generated at multiple sites on multiple vendor platforms are becoming more commonplace. The Ontario Neurodegenerative Disease Research Initiative (ONDRI -http://ondri.ca/), a project funded by the Ontario Brain Institute (OBI), is a recently established province-wide natural history study, which has recruited more than 500 participants from neurodegenerative disease groups including amyotrophic lateral sclerosis, fronto-temporal dementia, Parkinson's disease, Alzheimer's disease, mild cognitive impairment, and cerebrovascular disease (previously referred to as the vascular cognitive impairment cohort). Because of its multi-site nature, all captured data must be standardized and meet minimum quality standards to reduce variability. The goal of the ONDRI imaging platform is to maximize data quality by implementing vendor-specific harmonized MR imaging protocols (consistent with the Canadian Dementia Imaging Protocol -http://www.cdip-pcid.ca/), monitoring protocol adherence, qualitatively assessing image quality, measuring signal-to-noise and contrast-to-noise, monitoring system stability, and applying corrections based on the analysis of images from two different phantoms regularly acquired at each site. To maximize image quality, this work describes the use of various automatic pipelines and manual assessment steps, integrated within an established informatics and databasing platform, the Stroke Patient Recovery Research Database (SPReD) built on the Extensible Neuroimaging Archive Toolkit (XNAT), and contained within the Brain-CODE (Centre for Ontario Data Exploration) framework. The purpose of the current paper is to describe the steps undertaken by ONDRI to achieve this high standard of data integrity. Data have been successfully collected for the past 4 years with the pipelines and assessments identifying deviations, allowing for timely interventions and assessment of image quality.

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BackgroundRegional changes to cortical thickness in individuals with neurodegenerative and cerebrovascular diseases can be estimated using specialised neuroimaging software. However, the presence of cerebral small vessel disease, focal atrophy, and cortico-subcortical stroke lesions, pose significant challenges that increase the likelihood of misclassification errors and segmentation failures.PurposeThe main goal of this study was to examine a correction procedure developed for enhancing FreeSurfer’s cortical thickness estimation tool, particularly when applied to the most challenging MRI obtained from participants with chronic stroke and cerebrovascular disease, with varying degrees of neuro-vascular lesions and brain atrophy.MethodsIn 155 cerebrovascular disease patients enrolled in the Ontario Neurodegenerative Disease Research Initiative (ONDRI), FreeSurfer outputs were compared between a fully automated, unmodified procedure and a corrected procedure that accounted for potential sources of error due to atrophy and neurovascular lesions. Quality control (QC) measures were obtained from both procedures. Association between cortical thickness and global cognitive status as assessed by the Montreal Cognitive Assessment (MoCA) score was also investigated from both procedures.ResultsCorrected procedures increased ‘Acceptable’ QC ratings from 18% to 76% for the cortical ribbon and from 38% to 92% for tissue segmentation. Corrected procedures reduced ‘Fail’ ratings from 11% to 0% for the cortical ribbon and 62% to 8% for tissue segmentation. FreeSurfer-based segmentation of T1-weighted white matter hypointensities were significantly greater in the corrected procedure (5.8mL vs. 15.9mL, p<0.001). The unmodified procedure yielded no significant associations with global cognitive status, whereas the corrected procedure yielded positive associations between MoCA total score and clusters of cortical thickness in the left superior parietal (p=0.018) and left insula (p=0.04) regions. Further analyses with the corrected cortical thickness results and MoCA subscores showed a positive association between left superior parietal cortical thickness and Attention (p<0.001).ConclusionsThese findings suggest that correction procedures that account for brain atrophy and neurovascular lesions can significantly improve FreeSurfer’s segmentation results, reduce failure rates, and potentially increase sensitivity to examine brain-behaviour relationships. Future work will examine relationships between cortical thickness, cerebral small vessel disease, and neurodegenerative disease in the ONDRI study.

Background Cerebral small vessel disease is associated with higher ratios of soluble‐epoxide hydrolase derived linoleic acid diols (12,13‐dihydroxyoctadecenoic acid [DiHOME] and 9,10‐DiHOME) to their parent epoxides (12(13)‐epoxyoctadecenoic acid [EpOME] and 9(10)‐EpOME); however, the relationship has not yet been examined in stroke. Methods and Results Participants with mild to moderate small vessel stroke or large vessel stroke were selected based on clinical and imaging criteria. Metabolites were quantified by ultra‐high‐performance liquid chromatography–mass spectrometry. Volumes of stroke, lacunes, white matter hyperintensities, magnetic resonance imaging visible perivascular spaces, and free water diffusion were quantified from structural and diffusion magnetic resonance imaging (3 Tesla). Adjusted linear regression models were used for analysis. Compared with participants with large vessel stroke (n=30), participants with small vessel stroke (n=50) had a higher 12,13‐DiHOME/12(13)‐EpOME ratio (β=0.251, P =0.023). The 12,13‐DiHOME/12(13)‐EpOME ratio was associated with more lacunes (β=0.266, P =0.028) but not with large vessel stroke volumes. Ratios of 12,13‐DiHOME/12(13)‐EpOME and 9,10‐DiHOME/9(10)‐EpOME were associated with greater volumes of white matter hyperintensities (β=0.364, P <0.001; β=0.362, P <0.001) and white matter MRI‐visible perivascular spaces (β=0.302, P =0.011; β=0.314, P =0.006). In small vessel stroke, the 12,13‐DiHOME/12(13)‐EpOME ratio was associated with higher white matter free water diffusion (β=0.439, P =0.016), which was specific to the temporal lobe in exploratory regional analyses. The 9,10‐DiHOME/9(10)‐EpOME ratio was associated with temporal lobe atrophy (β=−0.277, P =0.031). Conclusions Linoleic acid markers of cytochrome P450/soluble‐epoxide hydrolase activity were associated with small versus large vessel stroke, with small vessel disease markers consistent with blood brain barrier and neurovascular‐glial disruption, and temporal lobe atrophy. The findings may indicate a novel modifiable risk factor for small vessel disease and related neurodegeneration.