Widespread Cortical Demyelination in Geriatric Cases of Mild Traumatic Brain Injury and in Alzheimer’s Disease

Abstract Cortical demyelination is related to neurodegeneration after mild traumatic brain injury (mTBI) and Alzheimer’s disease (AD). The ratio R of T1-to-T2-weighted magnetic resonance image (MRI) intensities is proportional to myelin content, and allows myelin changes to be mapped in vivo. T1 and T2 MRIs were acquired from mTBI patients (N = 97, age μ = 41 y; σ = 19 y, range: 21-79) both acutely and chronically (~1 week and ~6 months post-injury, respectively), from AD patients (N = 80, age μ = 76 y; σ = 8 y, range: 55-88), and from cognitively normal (CN) adults (N = 78, age μ = 75 y; σ = 5 y, range: 12-90). AD and CN subjects’ data were acquired less than a year apart. MRIs were analyzed using 3DSlicer’s BRAINSfit (registration), FreeSurfer (segmentation), SPM12 (bias field correction) and custom MATLAB scripts to calculate myelin content and demyelination. The null hypothesis of no myelin change was tested at each cortical location for each pair of groups (α = 0.05), after accounting for age, sex and interscan interval. Compared to HCs, AD subjects featured significantly greater myelin loss in dorsolateral prefrontal cortex, lateral and medial temporal lobes (~52% of the cortex, p < 0.05). mTBI participants experienced significantly greater myelin loss across ~96% of the cortex (p < 0.05), suggesting that mTBI has dramatic impact upon cortical myelin content. Myelin loss magnitude was comparable across mTBI and AD, particularly within temporal lobes. Future research should study whether post-traumatic demyelination increases the AD risk.

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Comparing Cortical Demyelination in Geriatric Mild Traumatic Brain Injury and Alzheimer’s Disease

Innovation in Aging ◽

10.1093/geroni/igab046.2406 ◽

2021 ◽

Vol 5 (Supplement_1) ◽

pp. 637-637

Author(s):

Shania Wang ◽

Nahian Chowdhury ◽

Sean Mahoney ◽

Andrei Irimia

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Traumatic Brain Injury ◽

Brain Injury ◽

Mild Traumatic Brain Injury ◽

Parietal Lobe ◽

Post Injury ◽

Temporal Lobes ◽

Magnetic Resonance Imaging Mri ◽

Time Changes

Abstract Mild traumatic brain injury (mTBI) accelerates the rate of age-associated brain atrophy, whose pattern resembles the cortical neurodegeneration pattern observed in Alzheimer’s disease (AD). Because the ratio R of T1-to-T2-weighted magnetic resonance imaging (MRI) intensities is a surrogate measure of cortical myelin concentration, mapping and quantifying changes in this ratio can improve our understanding of demyelination after geriatric mTBI and AD. T1- and T2-weighted MRIs were acquired acutely and ~6 months post-injury from 68 healthy controls (HCs, age (years, y): μ = 76 y, σ = 4 y), 19 mTBIs (age μ = 70 y, σ = 5 y), and 33 ADs (age μ = 77, σ = 6). Volumes were co-registered using 3D Slicer’s BRAINSFit module, and T2-constrained segmentations of T1 volumes were obtained using FreeSurfer. R and its time changes were computed at each cortical location. When comparing mTBI and AD patients to HCs, significant differences in R were found across ~10% and ~23% of the cortex, respectively (p < 0.05). When comparing mTBI to AD, the former exhibited significantly less myelin content in the lateral, medial, and ventral temporal lobes (p < 0.05), on the medial aspects of superior parietal lobules and superior frontal gyri (p < 0.05), and in orbital gyri (p < 0.05), whereas AD subjects had less myelin content on lateral aspect of the parietal lobe (p < 0.05). These results highlight demyelination differences in mTBI and AD. Future studies should examine the long-term trajectories to quantify the risk of neurodegenerative disease after mTBI.

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GERIATRIC TRAUMATIC BRAIN INJURY AND ALZHEIMER’S DISEASE SHARE SIMILAR PATTERNS OF WHITE MATTER DEGRADATION

Innovation in Aging ◽

10.1093/geroni/igz038.363 ◽

2019 ◽

Vol 3 (Supplement_1) ◽

pp. S96-S96

Author(s):

Andrei Irimia ◽

Kenneth Rostowsky ◽

Nikhil Chaudhari ◽

Maria Calvillo ◽

Sean Lee

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Traumatic Brain Injury ◽

Brain Injury ◽

White Matter ◽

Corpus Callosum ◽

Diffusion Tensor ◽

Future Research ◽

Post Injury ◽

Significant Difference

Abstract Although mild traumatic brain injury (mTBI) and Alzheimer’s disease (AD) are associated with white matter (WM) degradation, the nature of these alterations and the outcomes of their comparison have not been elucidated. Diffusion tensor imaging (DTI) has been utilized in both conditions, and has uncovered decreases in the fractional anisotropy (FA) of the corpus callosum and cingulum bundle, compared to healthy control (HC) volunteers [1, 2]. Despite mTBI being a potential risk factor for AD, no systematic quantitative comparison has been drawn between their WM degradation patterns. Here we investigated WM FA differences using DTI and tract-based spatial statistics (TBSS) between age- and sex-matched adults: 33 chronic mTBI patients, 67 AD patients and 81 HC participants. T1-weighted magnetic resonance imaging (MRI) and DTI were acquired at 3T. mTBI patients were scanned acutely and ~6 months post-injury. FSL software was used for artefact correction, FA computation and TBSS implementation. Statistical comparison of WM FA patterns between mTBI and AD patients was achieved by two one-sided t tests (TOSTs) of statistical equivalence, with equivalence bounds defined where Cohen’s d < 0.3. A significant difference was found between the FA means of mTBI vs. HC groups, and the AD vs. HC groups (p < 0.01, corrected). Mean FA differences between mTBI and AD were statistically equivalent in the corpus callosum and in the inferior longitudinal fasciculus (p < 0.05, corrected). Future research should focus on clarifying the similarities between mTBI and AD, potentially leading to novel hypotheses and improved AD diagnosis.

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