Spatial patterns of cortical demyelination in geriatric cases of traumatic brain injury and in Alzheimer's disease.

Abstract

Traumatic brain injury (TBI) causes demyelination and cortical neurodegeneration patterns similar to those of Alzheimer's disease (AD, Irimia et al. 2020). The ratio of T1 - to T2 -weighted magnetic resonance imaging (MRI) intensities is a measure of myelin content (Glasser & Van Essen, 2011). By mapping changes in this ratio, we report on the spatial and extent of demyelination after mild TBI (mTBI) relative to typical aging and AD. At two time points ∼6 months apart, T1 - and T2 -weighted MRIs were acquired from age- and sex-matched healthy control (HC) participants (N = 68; age (years): μ = 76.162, σ = 4.145), mTBI volunteers (N = 19; age: μ = 69.579. σ = 5.143), and AD patients (N = 33; age: μ = 77.420, σ = 5.545). After MRI coregistration, segmentation and bias field correction, the ratio R = T1 /T2 and its time change ΔR were computed at each cortical location. The null hypotheses that the means of ΔR were equal in (a) HCs vs. mTBI, (b) HCs and AD, and (c) mTBI vs. AD were tested (α = 0.05). Age effects were accounted for in statistical analyses. In the mTBI and AD groups, ∼10% and ∼23% of the cortex, respectively, exhibited significant decreases in R compared to HCs (p < 0.05); ∼7% of the cortex exhibited significantly larger myelin decreases in mTBI than in AD. mTBI subjects were found to have significantly less myelin than HCs in anterior limbic areas, the longitudinal frontal gyrus, left supplementary motor areas, and ventrolateral temporal regions. Compared to HCs, AD patients exhibited more demyelination across all lobes. mTBI subjects exhibited more demyelination than AD patients in temporal, supplementary motor, superior frontal, and orbitofrontal areas. Compared to mTBI, AD patients had significantly less myelin in parietal regions. Whereas demyelination occurs in both AD and geriatric mTBI, mTBI effect sizes are comparable to, or even greater than, those observed in AD. Future research should attempt to understand the long-term demyelination trajectories of mTBI relative to AD and leverage this information to forecast AD risk after geriatric TBI.