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Behind stress resilience: role of behavioral traits, neurochemical and neuroplasticity alterations

Resumo: Stressful life events are considered the main environmental factor associated with the emergence of psychiatric disorders. Interestingly, some people exposed to stress exhibit minimal and transient changes in their emotional well-being, while others develop impairments in quality of life, cognition, and psychiatric disorders. Our study will focus on the baseline assessment of memory and learning in male and female mice and their relationship with coping strategies and resilience or susceptibility to stress. We will focus on mechanisms associated with inflammation and autophagy and their interaction with neuroplasticity in specific areas regulating emotional behavior such as the cortex, hippocampus, nucleus accumbens and the amygdala. This knowledge can contribute to the understanding of brain circuits that regulate the response to stress, and to the development of pharmacological interventions in populations exposed to stress and the prevention of mental illnesses.

Financiamento: International Brain Research Organization (IBRO Connecting Regions Award); FAPESC.


CD300f receptors and neuroinflammation: potential effects in behavioral and neurochemical modifications associated to major depressive disorder.

Resumo: Depressive disorders affect more than 350 million people worldwide. Recently, increased immune responses and higher levels of inflammatory molecules have been found in depressed patients. The immune system is our defense system responsible for identifying and protecting the body against potential threats. However dysfunctional immune activation after stress exposure can be detrimental, and a condition called neuroinflammation may impact function and communication between brain cells in areas responsible for controlling behaviors such as mood and pleasure. Our goal is to study CD300f receptors, a molecule present in both immune and brain cells, involved in the control of immune activation and reduction of inflammation. We will use genetically modified mice and human studies in order to investigate if CD300f receptors can control the spread of neuroinflammation, changes in brain cells, and behavior. With this knowledge, we can propose new pharmacological strategies to treat depression.

Financiamento: Collaborative Research Program – ICGEB Research Grants 2019; CNPq Productivity in Research Fellowship to Manuella P. Kaster.


Molecular and biochemical markers in mental health

Resumo: Mental illnesses such as depression are pervasive, with as much as 26% of the American adult population suffering from these disorders each year. Despite the significant disease-related societal burden stemming from mental disorders, there remain significant gaps in our scientific understanding of the genesis, progression, and treatment of depression. One of the major drawbacks is that depression, like most of psychiatric disorders, is defined on the basis of behavioral modifications found in patients. There is currently no clear biomarker to support the modified behavioral patterns, the brain areas affected are rather broad and too many biochemical traits have been reported to be involved in this condition. The etiology of depression clearly involves multiple mechanisms such as dysfunction in the hypothalamic pituitary adrenal axis, in brain reward-seeking activities, emotion regulation circuits, in modulatory neurotransmitter systems, cognitive systems, and genetic/epigenetic marks. With this complexity it is not surprising that studies trying to establish the etiology of depression are equivocal and difficult to replicate, nor that new treatments directed toward a particular mechanism are often only marginally effective in patients. The goal of this multidisciplinary project will be to examine the association between particular features associated with depressive symptoms including anhedonia, alterations in circadian rhythms, dysfunction in motivation-reward systems, cognitive dysfunction and somatic alterations with genetic, and biochemical markers.

Financiamento: L’Oréal, UNESCO e ABC; CNPq Edital Universal 2016, FAPESC.