Purpose: White matter hyperintensities (WMH) and cerebral microbleeds (CMBs) are known to be associated with small vessel diseases (SVD) and neuroinflammation. The purpose was to investigate the relationship between CMBs and WMH in patients with systemic lupus erythematosus (SLE).
Methods: Thirty-one SLE patients with WMH and 27 SLE patients with normal brain MRI were compared. The presence, location, and grading of CMBs were assessed using susceptibility-weighted images. WMH volume was quantitatively measured. Clinical characteristics and serologic markers were compared. We also performed two separate subgroup analyses after (1) dividing WMH into inflammatory lesion vs. SVD subgroups and (2) dividing WMH into those with vs. without CMB subgroups.
Results: The WMH group showed more frequent CMBs than the normal MR group (p < 0.001). The WMH group showed higher SLE disease activity index, longer disease duration, and a higher incidence of antiphospholipid syndrome than the normal MR group (p = 0.02, 0.04, and 0.04, respectively). There was a moderate correlation between WMH volume and CMB grading (r = 0.49, p = 0.006). Within the WMH group, the inflammatory lesion subgroup showed more frequent CMBs and larger WMH volume than the SVD subgroup (p < 0.001 and 0.02, respectively). The WMH with CMB subgroup had larger WMH volume than the WMH without CMB subgroup (p = 0.004).
Conclusion: In patients with SLE, CMBs could be related to large-volume WMH and inflammatory lesions. CMBs along with severe WMH could be used as an imaging biomarker of vasculitis in patients with SLE.
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http://dx.doi.org/10.1007/s00234-018-2130-1 | DOI Listing |
Alzheimers Dement
December 2024
Bernard and Irene Schwartz Center for Biomedical Imaging, New York University Grossman School of Medicine, New York, NY, USA.
Background: Amyloid related imaging abnormalities (ARIA), a group of neuropathological features seen in anti-amyloid immunotherapy patients, arises partly from CAA (Aβ buildup in blood vessels). Squirrel monkeys (SQMs), developing prominent age-related CAA exceeding brain Aβ, offer a unique NHP model for ARIA study. Evaluating edema-related neurobiological defects (ARIA-E) involves preferential use of T-weighted (T-w) and flow-attenuated inversion recovery (FLAIR) MRI while T*-weighted (T*-w) MRI is better suited for investigating iron-related pathology like microbleeds, hemorrhaging, and iron-homing in plaques.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Neuroimage Analytics Laboratory and Glenn Biggs Institute Neuroimaging Core, Glenn Biggs Institute for Neurodegenerative Diseases, University of Texas Health San Antonio, San Antonio, TX, USA.
Background: The location of proposed brain MRI markers of small vessel disease (SVD) might reflect their pathogenesis and may translate into differential associations with cognition. We derived regional MRI markers of SVD and studied: (i) associations with cognitive performance, (ii) patterns most likely to reflect underlying SVD, (iii) mediating effects on the relationships of age and cardiovascular disease (CVD) risk with cognition.
Method: In 891 participants from The Multi-Ethnic Study of Atherosclerosis, we segmented enlarged perivascular spaces (ePVS), white matter hyperintensities (WMH) and microbleeds (MBs) using deep learning-based algorithms, and calculated white matter (WM) microstructural integrity measures of fractional anisotropy (FA), trace (TR) and free water (FW) using automated DTI-processing pipelines.
Alzheimers Dement
December 2024
Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Background: The identification of novel blood-based biomarkers of small vessel disease of the brain (SVD) may improve pathophysiologic understanding and inform the development of new therapeutic strategies for prevention. We evaluated plasma proteomic associations of white matter fractional anisotropy (WMFA), white matter hyperintensity (WMH) volume, enlarged perivascular space (ePVS) volume, and the presence of microbleeds (MB) on brain magnetic resonance imaging (MRI) in the population-based Multi-Ethnic Study of Atherosclerosis (MESA).
Methods: Eligible MESA participants had 2941 plasma proteins measured from stored blood samples (collected in 2016-2018) using the antibody-based Olink proteomics platform, and completed brain MRI scans in 2018-2019.
Alzheimers Dement
December 2024
Neurochemistry Laboratory, Department of Laboratory Medicine, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, North Holland, Netherlands.
Background: The exact mechanism underlying amyloid-related imaging abnormalities (ARIA) is unknown. Several factors explain ARIA risk, including the presence of microbleeds, APOE4 carriership, and very low Aβ42 levels. The cerebrospinal fluid (CSF) proteome reflects ongoing mechanisms and, thereby, provides an accessible fluid to refine risk of ARIA development.
View Article and Find Full Text PDFBackground: Sleep deficiency is associated with an increased risk of Alzheimer's disease (AD), warranting research on underlying mechanisms. This study examined the association of sleep architecture with anatomical features frequently observed in AD: (1) atrophy of cuneus, hippocampus, entorhinal, inferior parietal, parahippocampal, and precuneus regions (henceforth referred to as "AD-vulnerable regions") and (2) the presence of cerebral microbleeds.
Method: In 271 participants of the Atherosclerosis Risk in the Communities Study, we examined the prospective association of baseline sleep architecture with anatomical features of the brain identified on MRI conducted ∼17 years later.
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