Abstract
Mild traumatic brain injury (mTBI) initiating long-term effects on white matter integrity resembles brain-aging changes, implying an aging process accelerated by mTBI. This longitudinal study aims to investigate the mTBI-induced acceleration of the brain-aging process by developing a neuroimaging model to predict brain age. The brain-age prediction model was defined using relevance vector regression based on fractional anisotropy from diffusion tensor imaging of 523 healthy individuals. The model was used to estimate the brain-predicted age difference (brain-PAD) between the chronological and estimated brain age in 116 acute mTBI patients and 63 healthy controls. Fifty patients were followed for 6 ∼ 12 months to evaluate the longitudinal changes in brain-PAD. We investigated whether brain-PAD was greater in patients of older age, post-concussion complaints, and apolipoprotein E (APOE) ɛ4 genotype, and whether it had the potential to predict neuropsychological outcomes. The brain-age prediction model predicted brain age accurately (r = 0.96). The brains of mTBI patients in the acute phase were estimated to be "older," with greater brain-PAD (2.59 ± 5.97 years) than the healthy controls (0.12 ± 3.19 years) (p < 0.05), and remained stable 6-12 month post-injury (2.50 ± 4.54 years). Patients who were older or who had post-concussion complaints, rather than APOE ɛ4 genotype, had greater brain-PADs (p < 0.001, p = 0.024). Additionally, brain-PAD in the acute phase predicted information processing speed at the 6 ∼ 12 month follow-up (r = -0.36, p = 0.01). In conclusion, mTBI accelerates the brain-aging process, and brain-PAD may be capable of evaluating aging-associated issues post-injury, such as increased risks of neurodegeneration.
Highlights
Mild traumatic brain injury (TBI), accounting for 80 ~ 90% of the total TBI [1], is typically associated with microstructural integrity loss that persists chronically after the initial injury [2]
The majority of TBIs sustained in civilian contexts are within the mild range [14], which is associated with increased risks of dementia in older adults [15]
We investigated whether brain-PAD was prone to be greater in patients with elderly age, post-concussion complaints, and risky apolipoprotein E (APOE) genotype [15, 21,22,23], and whether it can predict the neuropsychological outcome for information processing speed (IPS)
Summary
Mild traumatic brain injury (TBI), accounting for 80 ~ 90% of the total TBI [1], is typically associated with microstructural integrity loss that persists chronically after the initial injury [2]. Cole et al observed a 4.66-year increase in brain-PAD estimated by morphometrics in white matter and a 5.97-year increase estimated by gray matter morphometrics in chronic moderate/severe TBI patients instead of the mild cases [10]. These results limited our understandings of how mTBI accelerated the brainaging process because only 17 patients with mTBI were included in their research. Long-term effects of mild traumatic brain injury (mTBI) resemble brain aging changes (i.e., microstructure integrity loss), which implies an accelerated age-associated process. This study aimed to develop a quantifiable neuroimaging marker to characterize the brain-aging process accelerated by mTBI from acute to chronic phases
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