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Microglia and their LAG3 checkpoint underlie the antidepressant and neurogenesis-enhancing effects of electroconvulsive stimulation

28 October, 2021
Microglia and their LAG3 checkpoint underlie the antidepressant and neurogenesis-enhancing effects of electroconvulsive stimulation

Despite evidence implicating microglia in the etiology and pathophysiology of major depression, there is paucity of information regarding the contribution of microglia-dependent molecular pathways to antidepressant procedures. In a new study Prof. Raz Yirmia, Dr. Neta Rimmerman and other members of the Laboratory for PsychoNeuroImmunology Research, investigated the role of microglia in a mouse model of depression (chronic unpredictable stress—CUS) and its reversal by electroconvulsive stimulation (ECS), by examining the effects of microglia depletion with the colony stimulating factor-1 antagonist PLX5622. Microglia depletion did not change basal behavioral measures or the responsiveness to CUS, but it completely abrogated the therapeutic effects of ECS on depressive-like behavior and neurogenesis impairment. Treatment with the microglia inhibitor minocycline concurrently with ECS also diminished the antidepressant and pro-neurogenesis effects of ECS. Hippocampal RNA-Seq analysis revealed that ECS significantly increased the expression of genes related to neurogenesis and dopamine signaling, while reducing the expression of several immune checkpoint genes, particularly lymphocyte-activating gene-3 (Lag3), which was the only microglial transcript significantly altered by ECS. None of these molecular changes occurred in microglia-depleted mice. Immunohistochemical analyses showed that ECS reversed the CUS-induced changes in microglial morphology and elevation in microglial LAG3 receptor expression. Consistently, either acute or chronic systemic administration of a LAG3 monoclonal antibody, which readily penetrated into the brain parenchyma and was found to serve as a direct checkpoint blocker in BV2 microglia cultures, rapidly rescued the CUS-induced microglial alterations, depressive-like symptoms, and neurogenesis impairment. These findings suggest that brain microglial LAG3 represents a promising target for novel antidepressant therapeutics.

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Clinical and Cognitive Insight in Pathological Anxiety

20 October, 2021
Clinical and Cognitive Insight in Pathological Anxiety

Although insight is widely studied in some disorders, research on insight in anxiety is limited. A New Study of Dr. Asala Halaj and Prof. Jonathan Huppert investigates clinical and cognitive insight and their relationship to symptoms and cognitive factors. A total of 175 participants with high trait anxiety completed an online self-reported measures and a reasoning task. No significant correlations between clinical and cognitive insight were found, suggesting the two constructs are distinct. Impaired clinical insight was significantly associated with reduced reports of symptoms, suggesting they are less likely to recognize that they have a problem. Impaired clinical insight was positively associated with negative metacognitive beliefs, suggesting they are likely to use unhelpful cognitions. Overall cognitive insight and self-reflection were positively associated with negative metacognition, suggesting that these individuals are more likely to have unhelpful metacognitive beliefs. Future research needs to explore the different constructs of insight and their relation to psychopathology and treatment outcomes in anxiety disorders.

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The roles of chronotype and time of day in predicting symptom fluctuations in obsessive-compulsive disorder using a daily-monitoring design

13 October, 2021
The roles of chronotype and time of day in predicting symptom fluctuations in obsessive-compulsive disorder using a daily-monitoring design

Do you or someone you know suffer from obsessive compulsive disorder (OCD)? Individuals with OCD experience intrusive and unwanted thoughts (e.g., “did I turn off the oven?”) along with strong urges to engage in behaviors meant to relieve the associated distress from the intrusive thoughts (e.g., repeatedly checking that the oven is turned off). As it turns out, certain individuals with OCD experience worse symptoms in the morning, while others later in the day. A new research of Hadar Naftalovich and Prof. Eyal Kalanthroff aims to answer: why? What factors impact when we feel better or when we feel worse throughout the day?

One possible explanation for these patterns has to do with one’s chronotype, which indicates one’s “biological clock”. Morning chronotypes tend to be more alert during the earlier hours of the day and less alert at night. The opposite is true for Evening types, who are more alert later in the day. Our alertness levels impact many aspects of our functioning, beyond just how awake or energetic we may feel, including our cognitive functioning. In this new paper Hadar and Eyal present findings that show that individuals with OCD tend to have worse symptoms during “nonoptimal” times of day based on their chronotype. In other words, Morning types will have worse symptoms at night and the opposite is true for Evening types. Using this knowledge, individuals can predict when their own symptoms may be easier or more challenging to manage. Clinicians can also use this knowledge to schedule sessions at optimal times for increasing the effectiveness of treatment and researchers use this to better understand the mechanisms behind these patterns to help improve current interventions. 

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What Is Social about Autism? The Role of Allostasis-Driven Learning

17 October, 2021
What Is Social about Autism? The Role of Allostasis-Driven Learning

A new Article by Dr. Shir Atzil and the students Meshi Djerassi and Shachar Ophir propose that autism is not the result of a broken "social brain". Instead, typical social development relies on allostasis-driven learning, and the most prominent learning in early life is crafted by social interactions. Therefore, the most prominent outcome of a learning variation is atypical social development. This new framework raises new research questions about the neural mechanisms underlying autism, and points to new targets for clinical intervention that can lower the age of diagnosis and improve the well-being of individuals with autism.

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