Methamphetamine is a potent psychostimulant that can induce psychosis among recreational and chronic users, with some users developing a persistent psychotic syndrome that shows similarities to schizophrenia. This review provides a comprehensive critique of research that has directly compared schizophrenia with acute and chronic METH psychosis, with particular focus on psychiatric and neurocognitive symptomatology. We conclude that while there is considerable overlap in the behavioral and cognitive symptoms between METH psychosis and schizophrenia, there appears to be some evidence that suggests there are divergent aspects to each condition, particularly with acute METH psychosis. Schizophrenia appears to be associated with pronounced thought disorder, negative symptoms more generally and cognitive deficits mediated by the parietal cortex, such as difficulties with selective visual attention, while visual and tactile hallucinations appear to be more prevalent in acute METH-induced psychosis. As such, acute METH psychosis may represent a distinct psychotic disorder to schizophrenia and could be clinically distinguished from a primary psychotic disorder based on the aforementioned behavioral and cognitive sequelae. Preliminary evidence, on the other hand, suggests that chronic METH psychosis may be clinically similar to that of primary psychotic disorders, particularly with respect to positive and cognitive symptomatology, although negative symptoms appear to be more pronounced in schizophrenia. Limitations of the literature and avenues for future research are also discussed.

These recommendations provide a coherent framework along with identified outcome instruments to guide psychosocial research in moderate-to-severe TBI. Adherence to the recommendations will enable data-pooling and comparison across studies and research settings facilitating consistent measurement across the lifespan.

Repeat administration of psychostimulants, such as methamphetamine, produces a progressive increase in locomotor activity (behavioral sensitization) in rodents that is believed to represent the underlying neurochemical changes driving psychoses. Alterations to the prefrontal cortex (PFC) are suggested to mediate the etiology and maintenance of these behavioral changes. As such, the aim of the current study was to investigate changes to protein expression in the PFC in male rats sensitized to methamphetamine using quantitative label-free shotgun proteomics. A methamphetamine challenge resulted in a significant sensitized locomotor response in methamphetamine pretreated animals compared to saline controls. Proteomic analysis revealed 96 proteins that were differentially expressed in the PFC of methamphetamine treated rats, with 20% of these being previously implicated in the neurobiology of schizophrenia in the PFC. We identified multiple biological functions in the PFC that appear to be commonly altered across methamphetamine-induced sensitization and schizophrenia, and these include synaptic regulation, protein phosphatase signaling, mitochondrial function, and alterations to the inhibitory GABAergic network. These changes could inform how alterations to the PFC could underlie the cognitive and behavioral dysfunction commonly seen across psychoses and places such biological changes as potential mediators in the maintenance of psychosis vulnerability.

In most Westernized societies, there has been an alarming increase in the consumption of sugar-sweetened drinks. For many adults these drinks represent a substantial proportion of their total daily caloric intake. Here we investigated whether extended exposure to sugar changes behavior and protein expression in the orbitofrontal cortex (OFC). Male adult Sprague-Dawley rats (n = 8 per group) were treated for 26 days with either water or a 10% sucrose solution. Locomotor behavior was measured on the first and last day of treatment, then 1 week after treatment. Following the 1-week period free from treatment, sucrose treated rats were significantly more active than the control. Two hours following final behavioral testing, brains were rapidly removed and prepared for proteomic analysis of the OFC. Label free quantitative shotgun proteomic analyses of three rats from each group found 290 proteins were differentially expressed in the sucrose treated group when compared to the control group. Major changes in the proteome were seen in proteins related to energy metabolism, mitochondrial function and the cellular response to stress. This research does not seek to suggest that sugar will cause specific neurological disorders, however similar changes in proteins have been seen in neurological disorders such as Alzheimer's disease, Parkinson's disease and schizophrenia.

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