Methamphetamine-associated cognitive decline is attenuated by neutralizing il-1 signaling

Publication date: Available online 15 March 2019Source: Brain, Behavior, and ImmunityAuthor(s): Arkadiusz Liśkiewicz, Marta Przybyła, Minseon Park, Daniela Liśkiewicz, Marta Nowacka-Chmielewska, Andrzej Małecki, Jarosław Barski, Joanna Lewin-Kowalik, Michal ToborekAbstractMethamphetamine (METH) abusers are prone to develop a variety of comorbidities, including cognitive disabilities, and the immunological responses have been recognized as an important component involved in the toxicity of this drug. Cytokines are among the key mediators between systemic inflammatory status and tissue responses. One of these, interleukin 1 (IL-1), has been hypothesized to be involved in cognitive functions and also appears to play a pivotal role among inflammatory molecules. In the present study, we demonstrate that exposure of mice to METH markedly increased the protein level of IL-1β in hippocampal tissue. Additionally, METH administration induced a decline in spatial learning and memory as determined by the Morris water maze test. We next evaluated the hypothesis that blocking IL-1β signaling can protect against METH-induced loss of cognitive functioning. The results indicated that METH-induced impaired spatial learning abilities were attenuated by co-administration of mouse IL-1 Trap, a dimeric fusion protein that incorporates the extracellular domains of both of the IL-1 receptor components required for IL-1 signaling (IL-1 receptor type 1 and IL-1 receptor accessory protein), link...
Source: Brain, Behavior, and Immunity - Category: Neurology Source Type: research