Distinct patterns of neurodegeneration after TBI and in Alzheimer's disease

Author:

Graham Neil S.N.12,Cole James H.34,Bourke Niall J.12,Schott Jonathan M.3,Sharp David J.125

Affiliation:

1. Department of Brain Sciences Imperial College London London UK

2. UK Dementia Research Institute Centre for Care Research and Technology at Imperial College London London UK

3. Dementia Research Centre UCL Queen Square Institute of Neurology London UK

4. Centre for Medical Image Computing UCL London UK

5. Centre for Injury Studies Imperial College London London UK

Abstract

AbstractIntroductionTraumatic brain injury (TBI) is a dementia risk factor, with Alzheimer's disease (AD) more common following injury. Patterns of neurodegeneration produced by TBI can be compared to AD and aging using volumetric MRI.MethodsA total of 55 patients after moderate to severe TBI (median age 40), 45 with AD (median age 69), and 61 healthy volunteers underwent magnetic resonance imaging over 2 years. Atrophy patterns were compared.ResultsAD patients had markedly lower baseline volumes. TBI was associated with increased white matter (WM) atrophy, particularly involving corticospinal tracts and callosum, whereas AD rates were increased across white and gray matter (GM). Subcortical WM loss was shared in AD/TBI, but deep WM atrophy was TBI‐specific and cortical atrophy AD‐specific. Post‐TBI atrophy patterns were distinct from aging, which resembled AD.DiscussionPost‐traumatic neurodegeneration 1.9–4.0 years (median) following moderate‐severe TBI is distinct from aging/AD, predominantly involving central WM. This likely reflects distributions of axonal injury, a neurodegeneration trigger.Highlights We compared patterns of brain atrophy longitudinally after moderate to severe TBI in late‐onset AD and healthy aging. Patients after TBI had abnormal brain atrophy involving the corpus callosum and other WM tracts, including corticospinal tracts, in a pattern that was specific and distinct from AD and aging. This pattern is reminiscent of axonal injury following TBI, and atrophy rates were predicted by the extent of axonal injury on diffusion tensor imaging, supporting a relationship between early axonal damage and chronic neurodegeneration.

Funder

GlaxoSmithKline

Wolfson Foundation

Alzheimer's Research Trust

Brain Research UK

Weston Brain Institute

Publisher

Wiley

Subject

Psychiatry and Mental health,Cellular and Molecular Neuroscience,Geriatrics and Gerontology,Neurology (clinical),Developmental Neuroscience,Health Policy,Epidemiology

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