Complex developmental trauma can lead to a host of psychological and behavioral issues in children. Trust-Based Relational Intervention (TBRI) is a therapeutic model that trains those who care for at-risk children to provide effective support and intervention. The one thing that almost all children experiencing trauma in any form have in common is that they are required to attend school. Teachers are the caregivers spending the most time with children second to their families, and in some cases, primary to their families. The effects of trauma are known to impact school behavior and performance. Children who have experienced trauma are more frequently referred for special education and disciplinary action, test lower than their peers, and fail out of school at a higher rates. Despite these unfortunate facts, research has shown that schools can help promote resilience to mitigate the effect trauma has on students by creating trauma-informed classrooms. The TBRI & Trauma-Informed Classroom training is an online training that is available to the general public. Participants who completed this training were surveyed in order to assess the quality and the outcomes of the training, as well as ways to improve comprehension and implementation. Understanding how this training is translating to practice is essential for future trainings. Creating trauma-informed classrooms that serve as places of healing for children who have experienced trauma is vital to the well-being of students who are in them.

Past research has shown that individuals can become self-radicalized (i.e., adopt more extreme attitudes in the absence of new information) by merely thinking about a group. The current experiment examined whether a specific type of thought, extrapolating from known to unknown group attributes, can also cause self-radicalization. To test this idea, half of the participants were instructed to extrapolate about attributes people who agreed and disagreed with them about a social topic might have, while a control group rated attributes unrelated to people who agreed and disagreed with them. Compared to control participants, extrapolators reported more negative attitudes toward people who disagreed with them and more positive attitudes toward people who agreed with them about whether abortion should be legal. Extremity of the extrapolated attributes also predicted more negative attitudes toward people who disagreed and more positive attitudes toward people who agreed with the extrapolator. The current findings add to past research and theory about the processes by which individuals can become self-radicalized.

Previous research in our lab has found that extrapolating from known to unknown attributes about a group can cause individuals to adopt more extreme attitudes (i.e., become self-radicalized) toward the group. The current study investigated whether individual differences in belief personification, or judging people based on their opinions, moderated the effects of extrapolation on self-radicalization toward people who agreed and disagreed with the extrapolator about a social topic. Compared to a control group, extrapolators reported more extreme attitudes toward people who agreed and disagreed with them about kneeling during the national anthem, and extremity of the extrapolated attributes predicted more extreme attitudes toward both groups. Self-radicalization was also strongest among extrapolators who expressed greater belief personification, whereas belief personification did not have an effect on the control condition. These results extend the understanding by which attitudes can become more extreme in the absence of new information.

Alzheimer’s disease (AD), the most common type of dementia, is a progressive neurodegenerative disease marked by memory loss and cognitive dysfunction due to protein aberrations in the brain. An estimated 5.8 million people in the U.S are currently living with this devastating disease, and no effective treatment exists. Furthermore, the etiology of AD remains largely unknown, though many risk factors have been identified. One such risk factor is experiencing chronic psychological stress. Over 77% of US adults report experiencing significant chronic stress. The current research aimed to explore the effects of chronic unpredictable stress on AD-like pathology in adult male C57BL/6 mice. Mice in the chronic unpredictable stress group were housed in isolation and were exposed to six different stressors presented at random for 21 consecutive days. These six stressors included being placed into a restraint tube, forced swimming in lukewarm water, being placed into an empty cage, cage being placed on a tilt, wet bedding, and removal of white bedding nestlet overnight. Mice in the control group remained in their group-housed cages and were not subjected to the stressors. During the final week of the paradigm, all mice received seven days of either lipopolysaccharide (LPS) or saline injections to explore whether an inflammatory insult would exacerbate the hypothesized detrimental effects of chronic unpredictable stress on AD-like pathology. Following the final day of stress and injections, all mice were trained in contextual fear conditioning, a Pavlovian learning paradigm to examine learning and memory. Following contextual fear conditioning, hippocampal tissue was collected to quantify amyloid-beta (Aβ), a protein which aggregates to form plaques that disrupt neuronal communication in AD. Although there were no effects of seven days of LPS injections on cognitive function or Aβ, chronic unpredictable stress was associated with impaired cognition and slightly increased hippocampal Aβ compared to the control condition. Further research is necessary to explore the mechanisms driving these observed differences. As the prevalence of AD is expected to continue to climb rapidly in the coming years, and, given the large percentage of the population reporting experiencing chronic stress, understanding how chronic stress may contribute to or exacerbate AD is crucial.

The current study aimed to investigate the neurobehavioral mechanisms underlying devaluation of expected rewards. In rats, frustration effects of reward loss are produced using the reward downshift (RD) situation. RD postshift phase involves two stages. After an initial suppression of sucrose consumption (Stage 1), behavior recovers to baseline levels (Stage 2). During Stage 1, nucleus accumbens (NAc) neurons release lower levels of dopamine, but it is not known whether they participate in the recovery process (Stage 2). We hypothesized that NAc activity would be important for the recovery process following a 32-2% sucrose downshift. The study explored the role of the NAc by selectively targeting both RD postshift stages using chemogenetics. Inhibitory or excitatory Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) were delivered into the NAc of rats via intracranial infusion and activated prior to downshift sessions via intraperitoneal injection of Clozapine N-Oxide (CNO), the activator drug for DREADDs. Rats were assigned to one of three neural manipulation condition, inhibition (INH), excitation (EXC), or control (CON), and received either CNO or Vehicle (veh) on postshift sessions. Thus, there were two groups in each neural manipulation condition: INH/CNO, INH/Veh, EXC/CNO, EXC/Veh, Control/CNO, and Control/Veh. Preliminary results revealed that NAc inhibition does not disrupt sucrose consumption during RD postshift. However, NAc excitation increases consummatory suppression and slows the recovery process. This pattern of results suggests that the chemogenetic manipulation may be affecting GABAergic projection neurons within the NAc, increasing the suppression of dopamine release, and resulting in suppressed behavioral response.