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Increased level of homocysteine is the cause of arteriosclerosis, vascular disorders, neurodegenerative diseases and mental disorders. This paper presents current views on hyperhomocysteinemia and its pathogenic role in mental disorders. The homocysteine metabolism is described as well as the influence of various factors on it, and also the pathomechanism of alterations resulting from an increased level of homocysteine. There is also a focus on genetic disorders leading to increased level of homocysteine and its correlation with mental disorders and dementia. The multidirectional influence of hyperhomocysteinemia on cardiovascular, immune and neurotransmitter systems is described as well as a neurotoxic action of homocysteine. Complex correlations between vitamin deficiency and hyperhomocysteinemia with depression, cognitive functions impairment and dementia are also presented. Oral supplementation with B-group vitamins and folic acid can significantly decrease a level of homocysteine in blood serum.

Glutamatergic system – main excitatory brain system is involved in pathophysiology of schizophrenia. Ionotropic glutamatergic NMDA receptor plays an important role in cognitive functioning and participates in mechanisms of control of dopaminergic, noradrenergic and serotoninergic systems. NMDA receptor antagonists as phencyclidyne or ketamine can induce psychosis similar to schizophrenia including also negative and cognitive symptomatology. Glycine is a natural coagonist of NMDA receptor necessary to its proper functioning. Treatment with high doses of glycine (max. 60g orally per day) according to hypothesis of decreased NMDA receptor activity can improve negative symptoms and cognitive functions in schizophrenia .
Purpose of the study: The aim of study was evaluation of changes in cognitive functioning of schizophrenic patients in stable mental state, with predominant negative symptoms (mean 25.7 points in PANSS-Negative symptom subscale), before and after 6-weeks augmentation of antipsychotic treatment with glycine.
Methods: 29 patients with diagnosis of schizophrenia (ICD-10 criterias) in stable clinical state had completed 6 weeks, prospective, open label study (32 patients were enrolled). Patients were treated with antipsychotics (typical and second generation neuroleptics) in stable dosage for at least 3 months. Before and afterwards glycine treatment (0,8 g/kg/day) cognitive functions were assessed with battery of standard neuropsychological tests: Wisconsin Card Sorting Test (WCST, version for PC), Trail Making Test (TMT) and Stroop Task. Clinical changes in negative symptoms were also assessed using PANSS-Negative symptom subscale.
Results: Improvement of working memory, attention and verbal functions after glycine treatment was significant in our group. In week 6 patients used less cards to finish more categories (p<0,001), making significantly fewer perseverative (p<0,001) and nonperseverative (p<0,01) errors. Afterwards glycine intake time needed to finish both parts of TMT was shorter (p<0,01). There was a significant decrease of numbers of errors and period of time necessary to finish second part of Stroop test, what indicates better verbal functioning and attention. Significant improvement in negative symptoms (PANSS-Negative symptom subscale; -16,1%; p<0,001) after use of glycine were observed.
Conclusions: Augmentation of antipsychotic treatment with glycine can improve cognitive functions and negative symptoms in schizophrenic patients. Combined medication was safe and well tolerated. Some patients complained on nausea or gastric discomfort.

Phenothiazine-derivatives (PHD) are the oldest and numerous group of neuroleptics with a potent antipsychotic effect. It's in common use, mainly in the treatment of psychiatric disorders. The aim of this study was to analyze fatal simple poisonings with PHD in the practice of the Chair and Department of Forensic Medicine and Forensic Toxicology, Medical University of Silesia in Katowice in the years 1999-2008. The results of chemico-toxicological investigations of biological material, collected during autopsies were analyzed, including sex of casualties, poisoning's circumstances (accident or suicide), the presence of medical indications for a drug intake, kind of it and its presence and concentration in examined material. PHD' identification doesn't produce any analytical problems. Poisonings with this group of neuroleptics consist still an essential toxicological problem, so patients should be under strict medical control during therapy. Fatal cases may constitute interpretative and opinion giving problems.

Neuroleptic treatment increases a risk of body weight gain. It seems the risk is highest during clozapine and olanzapine treatment. Body mass gain is shown in 57-58% of patients treated with olanzapine. Mechanisms of body mass gain, accompanying neuroleptic treatment are not fully understood and require further research.
Authors aimed at review of knowledge about appetite regulation and potential mechanisms of body weight gain with the special regard to olanzapine. Summary of pharmacological methods of prophylaxis and treatment of appetite increase, accompanying neuroleptic treatment is also presented.
Analysis of contemporary knowledge indicates that so for there is no convincing evidence of potential difference in an influence of orally dissolving pills and standard oral tablets forms of olanzapine on body weight gain. In relation to confirmed beneficial effect, correcting the orectic influence of olanzapine, further studies on metformin, topiramate, reboxetine and aripiprazole and perhaps on nizatidine and amantadine are necessary.

Nesfatin-1, a novel NUCB2-derived satiety peptide has a large distribution in numerous neurons of forebrain, hindbrain, brainstem and spinal cord. As a very potent anorexigenic substance seems to play a significant role in hypothalamic circuitries regulating food intake and energy homeostasis. On the other hand nesfatin-1 may be involved in other important brain functions such as sleep, cognition and anxiety- or stress-related responses. Nesfatin-1 is immunohistochemically detectable in arcuate (ARC), paraventricular (PVN) and supraoptic nuclei (SON), where the peptide is colocalized with POMC/CART, NPY, oxytocin and vasopressin. Nesfatin-1 interacts with a G-protein coupled receptor, its physiological effect depends on inhibitory hyperpolarization of NPY/AgRP neurons in ARC and melanocortin signaling in PVN. Administration of nesfatin-1 significantly inhibits consumatory behaviour and decreases weight gain in experimental animals. However, the details of nesfatin-1 physiology ought to be clarified, it will be useful in future as a potential drug in pharmacotherapy of obesity in patients treated with antipsychotics and antidepressants. Perhaps some putative nesfatin-1 antagonists may improve eating disorders e.g. anorexia nervosa.

The treatment of patients with epilepsy consists in taking antiepileptic drugs (AEDs), which may increase the concentration of homocysteine (Hcy), and alter metabolism of thiols. Increased Hcy levels in blood serum is known as hyperhomocysteinemia (HHcy). It is considered, that HHcy may cause DNA damage, oxidative stress and induce apoptosis. Hcy, is regarded as a risk factor for both neurodegenerative and cardiovascular diseases. First generation AEDs (mainly valproic acid – VPA) may induce apoptosis in many cancer cell lines by activating both intrinsic and extrinsic pathway, but also caspase-independent apoptotic signalling pathway. P53 protein may activate in cells caspase-dependent apoptotic pathway. Preliminary results may indicate increased proapoptotic effect in patients with epilepsy treatment AEDs as well.