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The back-to-back (BTB) acquisition of MP-RAGE MRI scans of the Alzheimer׳s Disease Neuroimaging Initiative (ADNI1) provides an excellent data set with which to check the reproducibility of brain atrophy measures. As part of ADNI1, 131 subjects received BTB MP-RAGEs at multiple time points and two field strengths of 3T and 1.5 T. As a result, high quality data from 200 subject-visit-pairs was available to compare the reproducibility of brain atrophies measured with FSL/SIENA over 12 to 18 month intervals at both 3T and 1.5 T. Although several publications have reported on the differing performance of brain atrophy measures at 3T and 1.5 T, no formal comparison of reproducibility has been published to date. Another goal was to check whether tuning SIENA options, including -B, -S, -R and the fractional intensity threshold (f) had a significant impact on the reproducibility. The BTB reproducibility for SIENA was quantified by the 50th percentile of the absolute value of the difference in the percentage brain volume change (PBVC) for the BTB MP-RAGES. At both 3T and 1.5 T the SIENA option combination of "-B f=0.2", which is different from the default values of f=0.5, yielded the best reproducibility as measured by the 50th percentile yielding 0.28 (0.23-0.39)% and 0.26 (0.20-0.32)%. These results demonstrated that in general 3T had no advantage over 1.5 T for the whole brain atrophy measure - at least for SIENA. While 3T MRI is superior to 1.5 T for many types of measurements, and thus worth the additional cost, brain atrophy measurement does not seem to be one of them.
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http://dx.doi.org/10.1016/j.pscychresns.2014.07.002 | DOI Listing |
Alzheimers Dement
September 2025
Department of Neurology, Beijing TianTan Hospital, Capital Medical University, Beijing, China.
Cognitive impairment and dementia, including Alzheimer's disease (AD), pose a global health crisis, necessitating non-invasive biomarkers for early detection. This review highlights the retina, an accessible extension of the central nervous system (CNS), as a window to cerebral pathology through structural, functional, and molecular alterations. By synthesizing interdisciplinary evidence, we identify retinal biomarkers as promising tools for early diagnosis and risk stratification.
View Article and Find Full Text PDFBrain Res Bull
September 2025
Department of Neurology, The Second Affiliated Hospital of Anhui Medical University, 230601, He Fei, China; Collaborative Innovation Center of Neuropsychiatric Disorders and Mental Health, 230032, Hefei, China; Anhui Province Key Laboratory of Cognition and Neuropsychiatric Disorders, 230032, Hefei,
Background: The relationships between white matter microstructure, cortical atrophy, and cognitive function in cerebral small vessel disease (CSVD)-related white matter hyperintensities (WMHs) patients are unclear.
Methods: 71 right-handed WMHs patients (mild, n=23; moderate, n=27; severe, n=21) and 35 healthy controls were included. Tract-based spatial statistics (TBSS) assessed microstructure via fractional anisotropy (FA) and mean diffusivity (MD).
Neurol Neuroimmunol Neuroinflamm
November 2025
Departments of Neurology and Ophthalmology, NYU Grossman School of Medicine, NY; and.
Background And Objectives: While reductions in optical coherence tomography (OCT) pRNFL and ganglion cell-inner plexiform layer thicknesses have been shown to be associated with brain atrophy in adult-onset MS (AOMS) cohorts, the relationship between OCT and brain MRI measures is less established in pediatric-onset MS (POMS). Our aim was to examine the associations of OCT measures with volumetric MRI in a cohort of patients with POMS to determine whether OCT measures reflect CNS neurodegeneration in this patient population, as is seen in AOMS cohorts.
Methods: This was a cross-sectional study with retrospective ascertainment of patients with POMS evaluated at a single center with expertise in POMS and neuro-ophthalmology.
J Alzheimers Dis
September 2025
Frontotemporal Disorders Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Compared with more typical late-onset Alzheimer's disease (AD), the mechanisms of young-onset AD (YOAD; age of symptom onset <65 years) remain less understood. Using resting-state functional MRI data and dynamic causal modeling techniques, Sacu et al. demonstrate that individuals with YOAD (amnestic AD or posterior cortical atrophy) exhibit alterations in effective (i.
View Article and Find Full Text PDFJCI Insight
September 2025
Edinburgh Medical School: Biomedical Sciences & Euan MacDonald Centre for M, University of Edinburgh, Edinburgh, United Kingdom.
Spinal muscular atrophy (SMA) is a neuromuscular disease caused by low levels of SMN protein. Several therapeutic approaches boosting SMN are approved for human patients, delivering remarkable improvements in lifespan and symptoms. However, emerging phenotypes, including neurodevelopmental comorbidities, are being reported in some treated SMA patients, indicative of alterations in brain development.
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