Journal
AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY
Volume 21, Issue 2, Pages 138-144Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1016/j.jagp.2012.11.019
Keywords
Positron emission tomography; FDDNP; tau; amyloid; mood disorder; depression; mild cognitive impairment; dementia
Categories
Funding
- Brain Injury Research Institute
- Fran and Ray Stark Foundation Fund for Alzheimer's Disease Research
- Ahmanson Foundation
- Parlow-Solomon Professorship
- Janssen
- Lilly
- Novartis
- Pfizer
- Nihon Medi-Physics Co
- Bristol-Meyer Squibb
- PETNet Pharmaceuticals
- Siemens
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Objective: Mild traumatic brain injury due to contact sports may cause chronic behavioral, mood, and cognitive disturbances associated with pathological deposition of tau protein found at brain autopsy. To explore whether brain tau deposits can be detected in living retired players, we used positron emission tomography (PET) scans after intravenous injections of 2-(1-{6-[(2-[F-18]fluoroethyl)(methyl)amino]-2-naphthyl}ethylidene)malononitrile (FDDNP). Methods: Five retired National Football League players (age range: 45 to 73 years) with histories of mood and cognitive symptoms received neuropsychiatric evaluations and FDDNP-PET PET signals in subcortical (caudate, putamen, thalamus, subthalamus, midbrain, cerebellar white matter) and cortical (amygdala, frontal, parietal, posterior cingulate, medial and lateral temporal) regions were compared with those of five male controls of comparable age, education, and body mass index. Results: FDDNP signals were higher in players compared with controls in all subcortical regions and the amygdala, areas that produce tau deposits following trauma. Conclusions: The small sample size and lack of autopsy confirmation warrant larger, more definitive studies, but if future research confirms these initial findings, FDDNP-PET may offer a means for premorbid identification of neurodegeneration in contact-sports athletes. (Am J Geriatr Psychiatry 2013; 21:138-144)
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