Substance-related psychopathology and aggressiveness in a nightlife holiday resort: Results from a pilot study in a psychiatric inpatient unit in Ibiza

Objectives: We aimed to describe a sample of subjects admitted to a psychiatric unit after the intake of psychoactive substances for recreational purposes. Methods: Between June and September 2015, 49 subjects were included. Sociodemographic characteristics and psychopathological aspects were investigated, and urine samples for further analysis were collected. Three subgroups (cannabinoids, stimulants, and depressors users) were identified, according to the structured interview regarding substance use and urinalysis. Results: Level of aggressiveness was found to be significantly higher (p <.05) in the cannabinoids subgroup. Self-reported symptom severity was comparable among groups, but trends could be identified: SCL-90 results showed a prevalence of anxiety symptoms among depressors users, hostility or aggression in the tetrahydrocannabinol subgroup, and psychoticism in the stimulants subgroup. Conclusions: The use of psychoactive substances was be characterised by poly-use of both traditional and novel substances. The presence of aggressiveness emerged as a main feature associated with the use of cannabis and other cannabinoids. Binge drinking and sleep deprivation also represented a relevant component in almost all the evaluated subjects

Party hard: Drug-related fatalities in Ibiza from 2010 to 2016

IntroductionIllicit drug use is well known as an important contributor to the global burden of diseases, but the physical and psychopathological risks of recreational drugs misuse are often underestimated and drug-related fatalities in specific settings are under-investigated.Objectives and methodsIn the framework of the EU-funded project “EU-Madness”, we collected and analysed all the reports of drug-related fatalities in Ibiza from January 2010 to September 2016, with the aim of characterising the sample, and identifying the involved substances and the nature of deaths associated with their consumption.ResultsOverall, 58 drug-related fatalities were registered from 2010 to September 2016 (87.9% males, 12.1% females, mean age 33.16; females were significantly younger than males). Most of the deceased were Britons (36.2%), followed by Spanish (22.4%), Italians (6.9%) and Germans (5.2%). In half the cases, the substance identified in post-mortem analyses was a stimulant; in 24.1% of the sample it was a depressor a prescription drug or more than two substances in 22.4%. Most of the fatalities were due to cardiovascular accidents (62%); 22.4% were deaths by drowning, 12% by fall from heights and 3.4% were due to mechanical asphyxia.ConclusionsAccording to the results from our sample, stimulants (mainly MDMA and cocaine) are the substances of abuse involved in most drug-caused fatalities. The number of fatalities per year has been steadily increasing, but the growing diffusion of novel psychoactive substances (NPS) does not seem to be a direct cause (although better methods of their analysis in post-mortem samples should be designed).Disclosure of interestThe authors have not supplied their declaration of competing interest.</jats:sec

A Phosphosite Mutant Approach on LRRK2 Links Phosphorylation and Dephosphorylation to Protective and Deleterious Markers, Respectively

The Leucine Rich Repeat Kinase 2 (LRRK2) gene is a major genetic determinant of Parkinson’s disease (PD), encoding a homonymous multi-domain protein with two catalytic activities, GTPase and Kinase, involved in intracellular signaling and trafficking. LRRK2 is phosphorylated at multiple sites, including a cluster of autophosphorylation sites in the GTPase domain and a cluster of heterologous phosphorylation sites at residues 860 to 976. Phosphorylation at these latter sites is found to be modified in brains of PD patients, as well as for some disease mutant forms of LRRK2. The main aim of this study is to investigate the functional consequences of LRRK2 phosphorylation or dephosphorylation at LRRK2’s heterologous phosphorylation sites. To this end, we generated LRRK2 phosphorylation site mutants and studied how these affected LRRK2 catalytic activity, neurite outgrowth and lysosomal physiology in cellular models. We show that phosphorylation of RAB8a and RAB10 substrates are reduced with phosphomimicking forms of LRRK2, while RAB29 induced activation of LRRK2 kinase activity is enhanced for phosphodead forms of LRRK2. Considering the hypothesis that PD pathology is associated to increased LRRK2 kinase activity, our results suggest that for its heterologous phosphorylation sites LRRK2 phosphorylation correlates to healthy phenotypes and LRRK2 dephosphorylation correlates to phenotypes associated to the PD pathological processes