RESUMO
Depression is a highly prevalent psychiatric condition, with over 300 million sufferers, and is an important comorbidity for other conditions, like cardiovascular disorders or diabetes. Therapy is largely based on psychotherapy and/or pharmacological intervention, particularly aimed at altering neurotransmitter levels in the central nervous system, but inadequate response to treatment remains a significant clinical problem. Herein, evidence supporting a molecular link between inflammation and depression will be discussed, particularly the increased prevalence of depression in chronic inflammatory diseases and the evidence on the use of anti-inflammatory drugs to treat depression. Moreover, the potential for the levels of peripheral inflammatory molecules to act as depression biomarkers, in the diagnosis and monitoring of depression will be examined, considering clinical- and animal model-based evidence.
Assuntos
Biomarcadores , Transtorno Depressivo/etiologia , Transtorno Depressivo/metabolismo , Modelos Animais de Doenças , Mediadores da Inflamação/metabolismo , Animais , Anti-Inflamatórios/farmacologia , Anti-Inflamatórios/uso terapêutico , Estudos Clínicos como Assunto , Citocinas , Depressão , Transtorno Depressivo/diagnóstico , Transtorno Depressivo/terapia , Humanos , Inflamação/complicações , Inflamação/tratamento farmacológico , Inflamação/etiologia , Inflamação/metabolismo , Resultado do TratamentoRESUMO
Autism comprises a complex and heterogeneous spectrum of neurodevelopmental disorders, usually termed autism spectrum disorders (ASD). It is more prevalent in males than females, and genetic and environmental factors are believed to account in similar percentages to the development of ASD. In recent years, the contribution of inflammation and inflammatory mediators to disease aetiology and perpetuation has been the object of intense research. In this chapter, inflammatory aspects that contribute to ASD are discussed, including abnormal microglia activation and polarization phenotypes, increased systemic levels of pro-inflammatory mediators, and altered patterns of immune cell response to activation stimuli. Also, inflammation in the context of gut microbiome and the impact of inflammation on gender prevalence of ASD are considered. Finally, treatment impact on inflammatory parameters and the potential for use of anti-inflammatory drugs, alone or in combination with antipsychotics, to manage ASD are examined.
