Studies for PTSD and Biological Aging
Cognitive and Neural Mechanisms of the Accelerated Aging Phenotype in PTSD
The purpose of this study is to investigate the relationship between aging processes and PTSD, which may help identify novel therapeutic targets to promote healthier aging trajectories for PTSD patients. Chronic PTSD increases mortality risk from medical diseases, promotes aging-associated syndromes such as frailty, and is linked to faster cognitive decline in older adults. One strong possibility is that PTSD leads to these adverse health outcomes by accelerating biological aging in the brain and body.
- Filling out forms
- Neuropsychological Testing
- Blood samples
- Ages eligible; 50 years and older
- Genders eligible: Both
- Exposure to trauma
For more information, please call Nicolas Cimino at 646-774-8655.
Comorbidity between posttraumatic stress disorder (PTSD) and major depressive disorder (MDD) has been commonly overlooked by studies examining resting-state functional connectivity patterns in PTSD. The current study used a data-driven approach to identify resting-state functional connectivity biomarkers to 1) differentiate individuals with PTSD (with or without MDD) from trauma-exposed healthy control subjects (TEHCs), 2) compare individuals with PTSD alone with those with comorbid PTSD+MDD, and 3) explore the clinical utility of the identified biomarkers by testing their associations with clinical symptoms and treatment response.
Posttraumatic stress disorder (PTSD) has been associated with altered resting-state functional connec-tivity (rs-FC) of several brain regions within the salience (SN) and default-mode (DMN) networks,including the hippocampus. However, most rs-FC studies have not focused primarily on the hippo-campus, nor have they appreciated its structural heterogeneity, despite clear evidence for a dissociationbetween posterior and anterior hippocampal connectivity. Here, we examine rs-FC of anterior andposterior hippocampus with key regions in the SN (amygdala, insula, and dorsal anterior cingulatecortex/pre-supplementary motor area) and DMN (ventromedial prefrontal cortex, posterior cingulatecortex, and precuneus) previously implicated in PTSD, using a seed-based approach. Resting-statemagnetic resonance images were obtained from 48 PTSD patients and 34 trauma-exposed healthyparticipants (TEHC). Results indicated no group differences when examining the hippocampus as awhole. However, examining the anterior and posterior hippocampus revealed a loss of anterior to pos-terior connectivity differentiation in PTSD patients. The PTSD group also demonstrated lower negativeconnectivity of the posterior hippocampus-precuneus pathway compared with the TEHC group. Finally,as differences in anterior and posterior hippocampus connectivity have been also related to age, weperformed a secondary analysis exploring the association between age and posterior- and anterior-hippocampus connectivity in both groups. Results showed that among PTSD patients, increased agehad the effect of normalizing posterior hippocampus-precuneus and hippocampus-posterior cingulatecortex connectivity, whereas no such effect was noted for the control group. Thesefindings highlight theneed for PTSD connectivity research to consider sub-parts of the hippocampus and to account for age-related connectivity differences.