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The primary objective of this study was to examine the impacts associated with implementation of overdose preventions sites (OPSs) in Victoria, Canada during a declared provincial public health overdose emergency. A rapid case study design was employed with three OPSs constituting the cases. Data were collected through semi-structured interviews with 15 staff, including experiential staff, and 12 service users. Theoretically, we were informed by the Consolidated Framework for Implementation Research. This framework, combined with a case study design, is well suited for generating insight into the impacts of an intervention. Zero deaths were identified as a key impact and indicator of success. The implementation of OPSs increased opportunities for early intervention in the event of an overdose, reducing trauma for staff and service users, and facilitated organizational transitions from provision of safer supplies to safer spaces. Providing a safer space meant drug use no longer needed to be concealed, with the effect of mitigating drug related stigma and facilitating a shift from shame and blame to increasing trust and development of relationships with increased opportunities to provide connections to other services. These impacts were achieved with few new resources highlighting the commitment of agencies and harm reduction workers, particularly those with lived experience, in achieving beneficial impacts. Although mitigating harms of overdose, OPSs do not address the root problem of an unsafe drug supply. OPSs are important life-saving interventions, but more is needed to address the current contamination of the illicit drug supply including provision of a safer supply.

The gene encoding for α-synuclein (SNCA) was the first to be linked to familial Parkinson's disease.1 At the same time, α-synuclein was identified as the main component of Lewy bodies, which are present in both familial and idiopathic Parkinson's disease.2 The Ala53Thr (A53T) SNCA mutation is associated with a similar clinical phenotype to the sporadic disease, albeit with earlier age-of-onset and faster disease progression.3,4 In The Lancet Neurology, Heather Wilson and colleagues5 report findings from a PET imaging study in A53T SNCA mutation carriers with (n=7) and without (n=7) clinically manifest Parkinson's disease, compared with patients with idiopathic Parkinson's disease (n=25)and healthy controls (n=25). The severity of the serotonin transporter loss in premotor carriers was noted to be at levels typically seen in idiopathic patients. [...]carriers with manifest disease showed greater loss of both serotonin and dopamine transporters in the caudate compared with age-matched idiopathic patients. Localised decreases in serotonergic transporter binding are a common finding in patients with Parkinson's disease, and have been associated with a variety of symptoms, including tremor and levodopa-mediated dyskinesias, and non-motor symptoms such as depression, fatigue, apathy, and weight changes.7 In the present study, brainstem serotonergic binding loss correlated with motor and non-motor symptoms in idiopathic Parkinson's disease patients and in A53T SNCA carriers with and without manifest disease.