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

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.

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

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 677-677
Author(s):  
Andrei Irimia ◽  
Nahian Chowdhury ◽  
Shania Wang ◽  
Sean Mahoney ◽  
Van Ngo ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Bias Field ◽  
Future Research ◽  
Post Injury ◽  
Temporal Lobes

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.

scholarly journals Age, Sex and Cerebral Microbleed Effects On White Matter Degradation After Traumatic Brain Injury

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 886-887
Author(s):  
Andrei Irimia ◽  
Ammar Dharani ◽  
Van Ngo ◽  
David Robles ◽  
Kenneth Rostowsky
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Diffusion Tensor ◽  
Diffuse Axonal Injury ◽  
Principal Component ◽  
Older Age ◽  
Analysis Of Covariance ◽  
Future Research ◽  
Cerebral Microbleed

Abstract Mild traumatic brain injury (mTBI) affects white matter (WM) integrity and accelerates neurodegeneration. This study assesses the effects of age, sex, and cerebral microbleed (CMB) load as predictors of WM integrity in 70 subjects aged 18-77 imaged acutely and ~6 months after mTBI using diffusion tensor imaging (DTI). Two-tensor unscented Kalman tractography was used to segment and cluster 73 WM structures and to map changes in their mean fractional anisotropy (FA), a surrogate measure of WM integrity. Dimensionality reduction of mean FA feature vectors was implemented using principal component (PC) analysis, and two prominent PCs were used as responses in a multivariate analysis of covariance. Acutely and chronically, older age was significantly associated with lower FA (F2,65 = 8.7, p < .001, η2 = 0.2; F2,65 = 12.3, p < .001, η2 = 0.3, respectively), notably in the corpus callosum and in dorsolateral temporal structures, confirming older adults’ WM vulnerability to mTBI. Chronically, sex was associated with mean FA (F2,65 = 5.0, p = 0.01, η2 = 0.1), indicating males’ greater susceptibility to WM degradation. Acutely, a significant association was observed between CMB load and mean FA (F2,65 = 5.1, p = 0.009, η2 = 0.1), suggesting that CMBs reflect the acute severity of diffuse axonal injury. Together, these findings indicate that older age, male sex, and CMB load are risk factors for WM degeneration. Future research should examine how sex- and age-mediated WM degradation lead to cognitive decline and connectome degeneration after mTBI.

scholarly journals Diffusion Tensor Imaging of the Evolving Response to Mild Traumatic Brain Injury in Rats

2019 ◽  
Vol 13 ◽  
pp. 117906951985862 ◽  
Author(s):  
Wouter S Hoogenboom ◽  
Todd G Rubin ◽  
Kenny Ye ◽  
Min-Hui Cui ◽  
Kelsey C Branch ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Diffusion Tensor Imaging ◽  
Brain Injury ◽  
White Matter ◽  
Mild Traumatic Brain Injury ◽  
Diffusion Tensor ◽  
Axonal Injury ◽  
Mean Diffusivity ◽  
Multiple Time ◽  
Post Injury

Mild traumatic brain injury (mTBI), also known as concussion, is a serious public health challenge. Although most patients recover, a substantial minority suffers chronic disability. The mechanisms underlying mTBI-related detrimental effects remain poorly understood. Although animal models contribute valuable preclinical information and improve our understanding of the underlying mechanisms following mTBI, only few studies have used diffusion tensor imaging (DTI) to study the evolution of axonal injury following mTBI in rodents. It is known that DTI shows changes after human concussion and the role of delineating imaging findings in animals is therefore to facilitate understanding of related mechanisms. In this work, we used a rodent model of mTBI to investigate longitudinal indices of axonal injury. We present the results of 45 animals that received magnetic resonance imaging (MRI) at multiple time points over a 2-week period following concussive or sham injury yielding 109 serial observations. Overall, the evolution of DTI metrics following concussive or sham injury differed by group. Diffusion tensor imaging changes within the white matter were most noticeable 1 week following injury and returned to baseline values after 2 weeks. More specifically, we observed increased fractional anisotropy in combination with decreased radial diffusivity and mean diffusivity, in the absence of changes in axial diffusivity, within the white matter of the genu corpus callosum at 1 week post-injury. Our study shows that DTI can detect microstructural white matter changes in the absence of gross abnormalities as indicated by visual screening of anatomical MRI and hematoxylin and eosin (H&E)-stained sections in a clinically relevant animal model of mTBI. Whereas additional histopathologic characterization is required to better understand the neurobiological correlates of DTI measures, our findings highlight the evolving nature of the brain’s response to injury following concussion.

281 Predicting neurodegeneration after traumatic brain injury

2018 ◽  
Vol 89 (10) ◽  
pp. A42.1-A42
Author(s):  
Graham Neil SN ◽  
Jolly Amy E ◽  
Bourke Niall J ◽  
Scott Gregory ◽  
Cole James H ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Brain Atrophy ◽  
Diffusion Tensor ◽  
Chronic Traumatic Encephalopathy ◽  
Axonal Injury ◽  
Diffuse Axonal Injury ◽  
Jacobian Determinant ◽  
Post Injury

BackgroundDementia rates are elevated after traumatic brain injury (TBI) and a subgroup develops chronic traumatic encephalopathy. Post-traumatic neurodegeneration can be measured by brain atrophy rates derived from neuroimaging, but it is unclear how atrophy relates to the initial pattern of injury.ObjectivesTo investigate the relationship between baseline TBI patterns and subsequent neurodegeneration measured by progressive brain atrophy.Methods55 patients after moderate-severe TBI (mean 3 years post-injury) and 20 controls underwent longitudinal MRI. Brain atrophy was quantified using the Jacobian determinant defined from volumetric T1 scans approximately one year apart. Diffuse axonal injury was measured using diffusion tensor imaging and focal injuries defined from T1 and FLAIR. Neuropsychological assessment was performed.ResultsAbnormal progressive brain atrophy was seen after TBI (~1.8%/year in white matter). This was accompanied by widespread reductions in fractional anisotropy, in keeping with the presence of diffuse axonal injury. There was a strong negative correlation between FA and brain atrophy, whereby areas of greater white matter damage showed greater atrophy over time.ConclusionsThe results show a strong relationship between the location of diffuse axonal injury and subsequent neurodegeneration. This suggests that TBI triggers progressive neurodegeneration through the long-lasting effects of diffuse axonal injury.

scholarly journals Refined Analysis of Chronic White Matter Changes after Traumatic Brain Injury and Repeated Sports-Related Concussions: Of Use in Targeted Rehabilitative Approaches?

2022 ◽  
Vol 11 (2) ◽  
pp. 358
Author(s):  
Francesco Latini ◽  
Markus Fahlström ◽  
Fredrik Vedung ◽  
Staffan Stensson ◽  
Elna-Marie Larsson ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Diffusion Tensor ◽  
Global Analysis ◽  
Memory Performance ◽  
Regional Analysis ◽  
Long Term Memory ◽  
Post Injury ◽  
White Matter Changes

Traumatic brain injury (TBI) or repeated sport-related concussions (rSRC) may lead to long-term memory impairment. Diffusion tensor imaging (DTI) is helpful to reveal global white matter damage but may underestimate focal abnormalities. We investigated the distribution of post-injury regional white matter changes after TBI and rSRC. Six patients with moderate/severe TBI, and 12 athletes with rSRC were included ≥6 months post-injury, and 10 (age-matched) healthy controls (HC) were analyzed. The Repeatable Battery for the Assessment of Neuropsychological Status was performed at the time of DTI. Major white matter pathways were tracked using q-space diffeomorphic reconstruction and analyzed for global and regional changes with a controlled false discovery rate. TBI patients displayed multiple classic white matter injuries compared with HC (p < 0.01). At the regional white matter analysis, the left frontal aslant tract, anterior thalamic radiation, and the genu of the corpus callosum displayed focal changes in both groups compared with HC but with different trends. Both TBI and rSRC displayed worse memory performance compared with HC (p < 0.05). While global analysis of DTI-based parameters did not reveal common abnormalities in TBI and rSRC, abnormalities to the fronto-thalamic network were observed in both groups using regional analysis of the white matter pathways. These results may be valuable to tailor individualized rehabilitative approaches for post-injury cognitive impairment in both TBI and rSRC patients.

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

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 &lt; 0.05). When comparing mTBI to AD, the former exhibited significantly less myelin content in the lateral, medial, and ventral temporal lobes (p &lt; 0.05), on the medial aspects of superior parietal lobules and superior frontal gyri (p &lt; 0.05), and in orbital gyri (p &lt; 0.05), whereas AD subjects had less myelin content on lateral aspect of the parietal lobe (p &lt; 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.

scholarly journals P4-305: GERIATRIC TRAUMATIC BRAIN INJURY AND ALZHEIMER'S DISEASE SHARE PATTERNS OF WHITE MATTER DECLINE

2019 ◽  
Vol 15 ◽  
pp. P1407-P1408 ◽  
Author(s):  
Kenneth A. Rostowsky ◽  
Nikhil N. Chaudhari ◽  
Maria Calvillo ◽  
Sean K. Lee ◽  
Andrei Irimia
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter

scholarly journals Acute cognitive deficits after traumatic brain injury predict Alzheimer's disease-like degradation of the human default mode network

2020 ◽  
Author(s):  
Andrei Irimia ◽  
Alexander S Maher ◽  
Nikhil N Chaudhari ◽  
Nahian F Chowdhury ◽  
Elliot B Jacobs
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Deficits ◽  
Default Mode Network ◽  
Brain Connectivity ◽  
The Elderly ◽  
Post Injury ◽  
Default Mode

Traumatic brain injury (TBI) and Alzheimer's disease (AD) are prominent neurological conditions whose neural and cognitive commonalities are poorly understood. The extent of TBI-related neurophysiological abnormalities has been hypothesized to reflect AD-like Neurodegeneration because TBI can increase vulnerability to AD. However, it remains challenging to prognosticate AD risk partly because the functional relationship between acute posttraumatic sequelae and chronic AD-like degradation remains elusive. Here, functional magnetic resonance imaging (fMRI), network theory, and machine learning (ML) are leveraged to study the extent to which geriatric mild TBI (mTBI) can lead to AD-like alteration of resting-state activity in the default mode network (DMN). This network is found to contain modules whose extent of AD-like, posttraumatic degradation can be accurately prognosticated based on the acute cognitive deficits of geriatric mTBI patients with cerebral microbleeds. Aside from establishing a predictive physiological association between geriatric mTBI, cognitive impairment, and AD-like functional degradation, these findings advance the goal of acutely forecasting mTBI patients' chronic deviations from normality along AD-like functional trajectories. The association of geriatric mTBI with AD-like changes in functional brain connectivity as early as ~6 months post-injury carries substantial implications for public health because TBI has relatively high prevalence in the elderly.

scholarly journals Age, Sex, and Cerebral Microbleeds Affect White Matter Integrity Across Adulthood After Mild Traumatic Brain Injury

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 829-829
Author(s):  
David Robles ◽  
Ammar Dharani ◽  
Nikhil Chaudhari ◽  
Kenneth Rostowsky ◽  
Layal Wehbe ◽  
...  
Keyword(s):  
Older Adults ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Diffusion Tensor ◽  
Cerebral Microbleeds ◽  
Future Research ◽  
Post Injury ◽  
Post Traumatic ◽  
Anterior Body

Abstract The contributions of age, sex, and cerebral microbleeds (CMBs) to WM changes after mild traumatic brain injury (mTBI) have not been studied. We used diffusion tensor imaging (DTI) to map WM fractional anisotropy (FA) changes across the first ~6 months post-mTBI in 109 subjects aged 18-77 (46 females; age µ: 40 y, σ: 17 y) imaged within ~1 week post-injury and ~6 months later. After partialing out age, sex, and CMB counts, significant mean FA decreases were found in the anterior body, posterior body, and splenium of the corpus callosum (CC; p = 0.003, 0.009 and 0.015, respectively), left superficial frontal fasciculus (p = 0.008), and left branch of the corticospinal tract (CST; p = 0.007). Age contributed to mean FAs measured acutely in the CC body (p = 0.04), and chronically in the CC genu (p &lt; 0.001), CC body (p = 0.01), and middle longitudinal fasciculi (p = 0.04), older adults exhibiting larger decreases. CMB counts were positively associated with mean FA decreases in the CC body (p = 0.04) and middle longitudinal fasciculi (p = 0.04). Significant age-by-sex and CMB count-by-age interactions mediated FA decreases in the CC genu (p = 0.02 and p = 0.03, respectively), older males exhibiting larger decreases. Thus, the CC, longitudinal fasciculi, superficial frontal WM and CST are particularly vulnerable to post-traumatic neurodegeneration moderated by age, sex and CMB count, men and older adults being at highest risk for adverse effects. Future research should investigate our findings relative to cognitive function.

Sign in / Sign up

Export Citation Format

Share Document