Affiliations: [a]
Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX, USA
| [b]
Department of Neurological Surgery, University of Texas Southwestern Medical Center, Dallas, TX, USA
| [c]
Department of Neurology, University of Texas Southwestern Medical Center, Dallas, TX, USA
| [d]
School of Behavioral and Brain Sciences, University of Texas at Dallas, Dallas, TX, USA
| [e]
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA
| [f]
Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA
Correspondence:
[*]
Correspondence to: Christian LoBue, PhD, 5323 Harry Hines Blvd., Dallas, TX 75390, USA. Tel.: +1 214 648 4646; Fax: +1 214 648 4660; E-mail: christian.lobue@utsouthwestern.edu.
Note: [1] Data used in preparation of this article were obtained from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database (http://adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in analysis or writing of this report. A complete listing of ADNI investigators can be found at:http://adni.loni.usc.edu/wpcontent/uploads/how_to_apply/AD_NI_Acknowledgement_List.pdf
Abstract: Few studies have examined an association between mild traumatic brain injury (mTBI) and Alzheimer’s disease (AD). For this reason, we compared an AD dementia group with an mTBI history (n = 10) to a matched AD control group (n = 20) on measures of cognitive function, cerebral glucose metabolism, and markers of amyloid and tau deposition. Only a trend and medium-to-large effect size for higher phosphorylated and total tau was identified for the mTBI group. A history of mTBI may be associated with greater tau in AD, indicating a potential pathway for increasing risk for AD, though further evaluation with larger samples is needed.
