Dyskinesias are involuntary muscle movements that occur spontaneously in Huntington's disease (HD) and after long-term treatments for Parkinson's disease (levodopa-induced dyskinesia; LID) or for schizophrenia (tardive dyskinesia, TD). Previous studies suggested that dyskinesias in these three conditions originate from different neuronal pathways that converge on overstimulation of the motor cortex. We hypothesized that the same variants of the N-methyl-D-aspartate receptor gene that were previously associated with the age of dyskinesia onset in HD were also associated with the vulnerability for TD and not LID. Genotyping patients with LID and TD revealed, however, that these two variants were dose-dependently associated with susceptibility to LID, but not TD. This suggested that LID, TD and HD might arise from the same neuronal pathways, but TD results from a different mechanism.

Myelin deficiency is commonly recognized as an important pathological feature of brain tissues in schizophrenia (SZ). In this pilot study, global myelin content abnormalities in white matter (WM) and gray matter (GM) of SZ patients were non-invasively investigated using a novel clinically-targeted quantitative myelin imaging technique, fast macromolecular proton fraction (MPF) mapping. MPF maps were obtained from 23 healthy subjects and 31 SZ patients using a clinical 1.5T magnetic resonance imaging (MRI) scanner. Mean MPF in WM and GM was compared between the healthy control subjects and SZ patients with positive and negative leading symptoms using the multivariate analysis of covariance. The SZ patients had significantly reduced MPF in GM (p < 0.001) and WM (p = 0.02) with the corresponding relative decrease of 5% and 3%, respectively. The effect sizes for the myelin content loss in SZ relative to the control group were 1.0 and 1.5 for WM and GM, respectively. The SZ patients with leading negative symptoms had significantly lower MPF in GM (p < 0.001) and WM (p = 0.003) as compared to the controls and showed a significant MPF decrease in WM (p = 0.03) relative to the patients with leading positive symptoms. MPF in WM significantly negatively correlated with the disease duration in SZ patients (Pearson’s r = −0.51; p = 0.004). This study demonstrates that chronic SZ is characterized by global microscopic brain hypomyelination of both WM and GM, which is associated with the disease duration and negative symptoms. Myelin deficiency in SZ can be detected and quantified by the fast MPF mapping method.

Schizophrenia is associated with a lowered life expectancy due to cardiovascular disease. This is, at least in part, related to an increased vulnerability to the development of metabolic syndrome (MetS) in patients with schizophrenia. The dysregulation of apolipoproteins (Apos) may also play a role in the pathogenesis of schizophrenia via their effect on cerebral cholesterol processing. The aim of this study was to investigate serum Apos A1, C3, E, A2 and C2 concentration in schizophrenia patients with or without MetS in comparison to healthy donors. After obtaining informed consent, 53 patients with a diagnosis of paranoid schizophrenia according to ICD-10 criteria (F20) were included. Patients were divided into two groups with (N = 26) and without (N = 27) MetS according to the criteria of the International Diabetes Federation. The control group included 20 mentally and physically healthy subjects. Serum Apos A1, A2, C2, C3 and E were measured using xMAP technology (Luminex). Serum ApoA1 was significantly decreased in patients with schizophrenia compared to healthy subjects (p = 0.002); ApoA2 was lower in patients without MetS in comparison to patients with MetS (p = 0.017) and the levels of ApoC3 and ApoC2 were increased in patients with schizophrenia with MetS in comparison with the control group and also with patients without MetS. No other significant differences were established concerning the other assayed apolipoproteins. In line with literature data the results of our study suggest that while disturbances in ApoA1 level may play a role in the pathogenesis of schizophrenia, ApoA2, ApoC2, ApoC3 and ApoE may be primarily related to metabolic imbalance.