Toxoplasma gondii is the etiologic agent of toxoplasmosis, a highly prevalent parasitosis. Toxoplasma gondii (T. gondii) transits in the brain from acute (AT) to chronic toxoplasmosis (CT), under host immune control. In immunocompromised patients, reactivation of CT is potentially life-threatening. Behavioral and neurological complications have been associated with CT. Furthermore, an effective treatment targeting CT is still lacking. We previously reported the efficacy of imiquimod against CT. Here, we demonstrate the molecular effects of imiquimod or imiquimod followed by the clinically used combination of sulfadiazine and pyrimethamine (SDZ + PYR) on CT-associated behavior in a rat model. Imiquimod decreased the number of cysts in the brains of chronically infected rats due to an induced reactivation of bradyzoites into tachyzoites. Importantly, this decrease was more pronounced in rats treated with imiquimod followed by SDZ + PYR. Rats chronically infected with T. gondii exhibited an anxiety-like behavior. Notably, treatment with imiquimod reversed this behavior aberrancy, with even a more pronounced effect with imiquimod followed by SDZ/PYR. Similarly, rats chronically infected with T. gondii exhibited learning deficits, and imiquimod alone or followed by SDZ/PYR reversed this behavior. Our results enhance our knowledge of the implications of CT on behavioral aberrancies and highlight the potency of imiquimod followed by SDZ + PYR on these CT-associated complications.

Vitamin D deficiency is a global problem. Vitamin D, the vitamin D receptor, and its enzymes are found throughout neuronal, ependymal, and glial cells in the brain and are implicated in certain processes and mechanisms in the brain. To investigate the processes affected by vitamin D deficiency in adults, we studied vitamin D deficient, control, and supplemented diets over 6 weeks in male and female C57Bl/6 mice. The effect of the vitamin D diets on proliferation in the neurogenic niches, changes in glial cells, as well as on memory, locomotion, and anxiety-like behavior, was investigated. Six weeks on a deficient diet was adequate time to reach deficiency. However, vitamin D deficiency and supplementation did not affect proliferation, neurogenesis, or astrocyte changes, and this was reflected on behavioral measures. Supplementation only affected microglia in the dentate gyrus of female mice. Indicating that vitamin D deficiency and supplementation do not affect these processes over a 6-week period.

Given the ambiguity surrounding traumatic brain injury (TBI) pathophysiology and the lack of any Food and Drug Administration (FDA)-approved neurotherapeutic drugs, there is an increasing need to better understand the mechanisms of TBI. Recently, the roles of inflammasomes have been highlighted as both potential therapeutic targets and diagnostic markers in different neurodegenerative disorders. Indeed, inflammasome activation plays a pivotal function in the central nervous system (CNS) response to many neurological conditions, as well as to several neurodegenerative disorders, specifically, TBI. This comprehensive review summarizes and critically discusses the mechanisms that govern the activation and assembly of inflammasome complexes and the major methods used to study inflammasome activation in TBI and its implication for other neurodegenerative disorders. Also, we will review how inflammasome activation is critical in CNS homeostasis and pathogenesis, and how it can impact chronic TBI sequalae and increase the risk of developing neurodegenerative diseases. Additionally, we discuss the recent updates on inflammasome-related biomarkers and the potential to utilize inflammasomes as putative therapeutic targets that hold the potential to better diagnose and treat subjects with TBI.

Neurophysiologic anomalies in major depressive disorder (MDD) have been characterized using electroencephalography (EEG) and functional imaging. In healthy persons, occipital alpha oscillations are thought to indicate top-down inhibition of the visual system, particularly visual attention. Different patterns of occipital alpha or altered relationships of alpha to relevant network activity could reflect connectivity deficits that impact visual processing and attention in MDD.

Background: Schizophrenia is often associated with poor clinical insight (unawareness of mental illness and its symptoms) and deficits in empathy, which are important for social functioning. Cognitive empathy has been linked to clinical insight while affective empathy and its role in insight and pathology have received mixed evidence. Methods: Instruments assessing symptomatology (Positive and Negative Syndrome Scale; PANSS), clinical insight (Scales to assess awareness of mental disorders; SUMD), and cognitive and affective empathy were administered to 22 participants with first episode and chronic schizophrenia and 21 healthy controls. Self-report, parent-report, and performance based measures were used to assess cognitive and affective empathy (The interpersonal reactivity index; IRI/Reading the Mind in the Eyes Test/Faux Pas) to reduce bias and parse shared variance. Results: Age of onset, gender, and symptomatology emerged as significant predictors of poor clinical insight. Additionally, the fantasy subscale of the IRI as reported by parents emerged as a positive predictor while the personal distress (parent report) subscale emerged as a negative predictor of awareness into mental illness. There were significant differences on performance-based measures of empathy between the control and schizophrenia groups. Conclusion: Findings suggest that affective empathy is relatively intact across phases of illness whereas cognitive empathy abilities are compromised and could be targets for psychotherapy intervention.

Electroconvulsive therapy (ECT) efficacy and cognitive side effects remain influenced by several parameters including electrodes position and configuration, the applied current intensity, duration, and polarity. We report on latest development in FEAST and its mechanisms of actions.