Traumatic brain injury fast-forwards Alzheimer's pathology: evidence from amyloid positron emission tomorgraphy imaging.

Mohamed, Abdalla Z; Nestor, Peter J; Cumming, Paul; Nasrallah, Fatima A (2022). Traumatic brain injury fast-forwards Alzheimer's pathology: evidence from amyloid positron emission tomorgraphy imaging. Journal of neurology, 269(2), pp. 873-884. Springer 10.1007/s00415-021-10669-5

[img] Text
Mohamed2021_Article_TraumaticBrainInjuryFast-forwa.pdf - Published Version
Restricted to registered users only
Available under License Publisher holds Copyright.

Download (1MB) | Request a copy

PURPOSE

Traumatic brain injury (TBI) has been proposed as a risk factor for Alzheimer's disease (AD), although the mechanisms underlying the putative association are poorly understood. We investigated elderly individuals with a remote history of TBI, aiming to understand how this may have influenced amyloidosis, neurodegeneration, and clinical expression along the AD continuum.

METHODS

Total of 241 individual datasets including amyloid beta (Aβ) positron emission tomography ([18F]-AV45), structural MRI, and neuropsychological measures, were obtained from the Alzheimer's Disease Neuroimaging Initiative. The data were stratified into groups with (TBI +) or without (TBI -) history of head injury, and by clinical dementia rating (CDR) scores, into subgroups with normal cognition (CDR = 0) and those with symptomatic cognitive decline (CDR ≥ 0.5). We contrasted the TBI + and TBI - subgroups with respect to the onset age and extent of cognitive decline, cortical thickness changes, and Aβ standard uptake value (SUVr).

RESULTS

Compared to the TBI -/CDR ≥ 0.5 subgroup, the TBI + /CDR ≥ 0.5 subgroup showed a 3-4 year earlier age of cognitive impairment onset (ACIO, p = 0.005). Among those participants on the AD continuum (Aβ + , as defined by a cortical SUVr ≥ 1.23), irrespective of current CDR, a TBI + history was associated with greater Aβ deposition and more pronounced cortical thinning. When matched for severity of cognitive status, the TBI + /CDR ≥ 0.5 group showed greater Aβ burden, but earlier ACIO as compared to the TBI -/CDR ≥ 0.5, suggesting a more indolent clinical AD progression in those with TBI history.

CONCLUSION

Remote TBI history may alter the AD onset trajectory, with approximately 4 years earlier ACIO, greater amyloid deposition, and cortical thinning.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Department of Radiology, Neuroradiology and Nuclear Medicine (DRNN) > Clinic of Nuclear Medicine

UniBE Contributor:

Cumming, Paul

Subjects:

600 Technology > 610 Medicine & health

ISSN:

1432-1459

Publisher:

Springer

Language:

English

Submitter:

Daria Vogelsang

Date Deposited:

07 Jan 2022 10:16

Last Modified:

05 Dec 2022 15:55

Publisher DOI:

10.1007/s00415-021-10669-5

PubMed ID:

34191080

Uncontrolled Keywords:

Alzheimer’s Disease Neuroimaging Initiative (ADNI) Alzheimer’s disease Amyloid Traumatic brain injury Voxel-based morphometry [18F]-AV45 PET

BORIS DOI:

10.48350/161796

URI:

https://boris.unibe.ch/id/eprint/161796

Actions (login required)

Edit item Edit item
Provide Feedback