PMC:7463108 / 8030-9622 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7463108","sourcedb":"PMC","sourceid":"7463108","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7463108","text":"For delayed heroin overdose death after a survival period of 5 h or more, studies report neurovascular disorders, hypoxic ischemic leukoencephalopathy, and region-specific atrophy with neuronal losses that can include the hippocampal formation, the cerebellar Purkinje cell layer and olivary nucleus (Protass 1971; Ginsberg et al. 1976; Gosztonyi et al. 1993), as well as other areas (Buttner 2011; Cadet et al. 2014). Loss of neurons and synaptic connections is supported by postmortem reports of smaller mean relative volumes in various brain regions in individuals with OUD, including cortical areas (Danos et al. 1998; Pezawas et al. 1998), the basal ganglia (Muller et al. 2015, 2019), prefrontal cortex (Cadet et al. 2014), and hypothalamus (Muller et al. 2018). Interestingly, leukoencephalopathy, atrophy (Cadet et al. 2014), and increased hyperphosphorylated tau-containing neurofibrillary tangles are reported with chronic opiate abuse compared to age-matched controls (Ramage et al. 2005; Anthony et al. 2010; Kovacs et al. 2015). Glycogen synthase kinase 3 α or β (GSK-3α/β; the pan antibody used in this study does not discern α from β isoforms) and/or cyclin-dependent kinase-5 (Cdk-5) are increased in the frontal and temporal cortices, the locus coeruleus, and the hippocampus, respectively, and correlate with microgliosis (Anthony et al. 2010). Further, more prolonged use increases the risk of accelerated age-related and even Alzheimer’s-like pathological changes (Ramage et al. 2005; Anthony et al. 2010; Kovacs et al. 2015) and cognitive impairment (Gruber et al. 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