Polish Road Toward an Illiberal State: Methods and Resistance

Since 2015, Poland has experienced a backsliding in democratic and rule of law standards. The ruling party, “Law and Justice,” has adopted a series of legislative changes affecting the independence of courts and checks and balances mechanisms. Some reforms were copied from Hungary, which, as the first Member State of the European Union, started the way toward illiberal democracy in contemporary Europe. Despite pressure from international organizations, the process of changes in Poland did not stop. However, it is important to look at methods implemented to dismantling democracy, as they can be used in other countries. This paper also analyzes different forms of domestic and international resistance toward non-democratic changes, including the special role of civil society and lawyers, as well as monitoring and judicial mechanisms used by the European Union

Depression Following a Traumatic Brain Injury: Uncovering Cytokine Dysregulation as a Pathogenic Mechanism

A substantial number of individuals have long-lasting adverse effects from a traumatic brain injury (TBI). Depression is one of these long-term complications that influences many aspects of life. Depression can limit the ability to return to work, and even worsen cognitive function and contribute to dementia. The mechanistic cause for the increased depression risk associated with a TBI remains to be defined. As TBI results in chronic neuroinflammation, and priming of glia to a secondary challenge, the inflammatory theory of depression provides a promising framework for investigating the cause of depression following a TBI. Increases in cytokines similar to those seen in depression in the general population are also increased following a TBI. Biomarker levels of cytokines peak within hours-to-days after the injury, yet pro-inflammatory cytokines may still be elevated above physiological levels months-to-years following TBI, which is the time frame in which post-TBI depression can persist. As tumor necrosis factor α and interleukin 1 can signal directly at the neuronal synapse, pathophysiological levels of these cytokines can detrimentally alter neuronal synaptic physiology. The purpose of this review is to outline the current evidence for the inflammatory hypothesis of depression specifically as it relates to depression following a TBI. Moreover, we will illustrate the potential synaptic mechanisms by which tumor necrosis factor α and interleukin 1 could contribute to depression. The association of inflammation with the development of depression is compelling; however, in the context of post-TBI depression, the role of inflammation is understudied. This review attempts to highlight the need to understand and treat the psychological complications of a TBI, potentially by neuroimmune modulation, as the neuropsychiatric disabilities can have a great impact on the rehabilitation from the injury, and overall quality of life