Abstract
BackgroundNeuroinflammation has long been theorized to arise from exposures to fine particulate matter and to be modulated when individuals experience chronic stress, both of which are also though to cause cognitive decline in part as a result of neuroinflammation. ObjectivesHypothesizing that neuroinflammation might be linked to experiences at the World Trade Center (WTC) events, this study explored associations between glial activation and neuropsychological measures including post-traumatic stress disorder (PTSD) symptom severity and WTC exposure duration. MethodsTranslocator protein 18-kDa (TSPO) is overexpressed by activated glial cells, predominantly microglia and astrocytes, making TSPO distribution a putative biomarker for neuroinflammation. Twenty WTC responders completed neuropsychological assessments and in vivo PET brain scan with [18F]-FEPPA. Generalized linear modeling was used to test associations between PTSD, and WTC exposure duratiioni as the predictor and both global and regional [18F]-FEPPA total distribution volumes as the outcomes. ResultResponders were 56.0 ± 4.7 years-old, and 75% were police officers on 9/11/2001, and all had at least a high school education. Higher PTSD symptom severity was associated with global and regional elevations in [18F]-FEPPA binding predominantly in the hippocampus (d = 0.72, P = 0.001) and frontal cortex (d = 0.64, P = 0.004). Longer exposure duration to WTC sites was associated with higher [18F]-FEPPA binding in the parietal cortex. ConclusionFindings from this study of WTC responders at midlife suggest that glial activation is associated with PTSD symptoms, and WTC exposure duration. Future investigation is needed to understand the important role of neuroinflammation in highly exposed WTC responders.
Highlights
During the World Trade Center (WTC) attacks on 9/11/2001 and in their aftermath, the responders who aided in the search, rescue, and recovery efforts endured multiple traumatic and toxic environmental exposures (Dasaro et al, 2017)
Our results revealed significant associations between post-traumatic stress disorder (PTSD) symptom severity and higher [18F]-FEPPA binding, predominantly in the hippocampus and frontal cortex, and longer WTC exposure duration was associated with higher Translocator protein 18-kDa (TSPO) binding in the parietal cortex
We found that higher PTSD symptom severity was associated with global and regional elevations in [18F]-FEPPA binding in most region of interest (ROI) measured with the strongest associations observed in the hippocampus and frontal cortex
Summary
During the World Trade Center (WTC) attacks on 9/11/2001 and in their aftermath, the responders who aided in the search, rescue, and recovery efforts endured multiple traumatic and toxic environmental exposures (Dasaro et al, 2017). The men and women who participated in search, rescue, and recovery operations on the event were exposed to severe physical exposures and stressful experiences (Galea et al, 2002). Objectives: Hypothesizing that neuroinflammation might be linked to experiences at the World Trade Center (WTC) events, this study explored associations between glial activation and neuropsychological measures including post-traumatic stress disorder (PTSD) symptom severity and WTC exposure duration. Higher PTSD symptom severity was associated with global and regional elevations in [18F]-FEPPA binding predominantly in the hippocampus (d 1⁄4 0.72, P 1⁄4 0.001) and frontal cortex (d 1⁄4 0.64, P 1⁄4 0.004). Conclusion: Findings from this study of WTC responders at midlife suggest that glial activation is associated with PTSD symptoms, and WTC exposure duration. Future investigation is needed to understand the important role of neuroinflammation in highly exposed WTC responders
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