Brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT3) levels in post-mortem brain tissue from patients with depression compared to healthy individuals - a proof of concept study.

The neurotrophic factors (NTF) hypothesis of depression was postulated nearly a decade ago and is nowadays widely acknowledged. Previous reports suggest that cerebral concentrations of NTF may be reduced in suicide victims who received minimal or no antidepressant pharmacotherapy. Recent evidence suggests that antidepressant treatment may improve or normalise cerebral concentrations of neurotrophic factors. Therefore, we examined the concentration of brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT3) in different brain regions (cortex, cingulate gyrus, thalamus, hippocampus, putamen and nucleus caudatus) of 21 individuals - 7 patients of which 4 patients with major depressive disorder (MDD) and overall age 86.8±5 years who received antidepressant pharmacotherapy (selective serotonin re-uptake inhibitors [SSRI]; tricyclic antidepressants [TCA]), 3 patients with MDD without antidepressant treatment and overall age 84.3±5 years versus 14 unaffected subjects at age 70.3±13.8. We detected significant elevation of BDNF (parietal cortex) and NT3 (parietal, temporal and occipital cortex, cingulate gyrus, thalamus, putamen and nucleus caudatus regions) in MDD patients who received antidepressant medication compared to MDD untreated patients and controls. Moreover, we detected a significant decrease of NT3 levels in the parietal cortex of patients suffering from MDD non-treated patients without treatment compared to healthy individuals. Although the limited statistical power due to the small sample size in this proof of concept study corroborates data from previous studies, which show that treatment with antidepressants mediates alterations in neuroplasticity via the action of NTF. However, more research using post-mortem brain tissue with larger samples needs to be carried out as well as longitudinal studies to further verify these results.

Altered serum mono- and polyunsaturated fatty acid levels in adults with ADHD.

Other than in children diagnosed with attention deficit hyperactivity disorder (ADHD), the connection between ADHD and lipids has not been sufficiently investigated so far in adults. Blood serum lipoproteins and fatty acids (FA) composition were measured and analyzed by colorimetry and gaschromatography in eight male and seven female adults diagnosed with ADHD as well as in 15 age- and gender-matched healthy control subjects. In ADHD patients, polyunsaturated FAs [docosahexaenoic, arachidonic and dihomogammalinolenic acid (p = 0.048; 0.003; 0.012)] showed lower concentrations, while monounsaturated acids (palmitoleic and oleic acid) as well as total and LDL cholesterol showed higher concentrations (p = 0.011; 0.005). ADHD scores positively correlated with palmitoleic (R = -0.56; p = 0.032), stearic (R = 0.53; p = 0.044), eicosapentaenoic (R = 0.62; p = 0.014), docosahexaenoic (R = 0.51; p = 0.050), gammalinolenic (R = 0.62; p = 0.018) and alphalinolenic acid (R = 0.56; p = 0.031) concentration. Even though the total and LDL cholesterol concentrations in blood serum were significantly higher among the ADHD patients than in controls, none of the ADHD symptom scores were significantly associated with any of the lipoproteine measures. We could demonstrate that a lack of polyunsaturated FAs in blood serum of subjects with ADHD persists into adulthood. Furthermore, we could show that adult ADHD symptomatology positively correlates with elevated levels of saturated stearic and monounsaturated FAs.

[Evaluation of diagnostic and therapeutic services in German university hospitals for adults with autism spectrum disorder (ASD)]. / Evaluation diagnostischer und therapeutischer Angebote deutscher Universitätskliniken für Patienten mit Autismus-Spektrum-Störungen (ASD) im Erwachsenenalter.

INTRODUCTION: Autism spectrum disorders (ASD), are pervasive developmental disorders, which are defined by qualitative impairment in reciprocal social interaction and communication as well as by stereotyped repetitive behaviour. Newer epidemiological studies report a prevalence of 1 %. However, parents and self-help organisations report a considerable lack of diagnostic services, especially in the university hospital setting. In order to receive funding for adequate treatment at an "autism therapy centre", a Consultant psychiatrist has to diagnose ASD. METHODS: We assessed the diagnostic and therapeutic facilities for adults with ASD by sending out questionnaires to 33 German university hospitals. Furthermore, we evaluated the demographic data of the first 74 patients that presented at the specialist clinic for adults with ASD at the Department for Psychiatry and Psychotherapy, RWTH Aachen University. RESULTS: At the time of the evaluation, only 9 university hospitals in Germany offered a specialist clinic for diagnostics and/or treatment for adults with ASD. A comorbid psychiatric disorder was diagnosed in 52.9 % of the patients presenting at the specialist clinic for adult ASD. These were mostly mental retardation and affective disorders. The most common differential diagnosis for the patients presenting at the service were affective and personality disorders. CONCLUSION: There is still great need of specialist services at university hospitals in Germany for adults with ASD, although more services have been established over the past few years. Over half of the patients with ASD had other psychiatric comorbid disorders, which were mostly mental retardation and affective disorders. The most common differential diagnosis for patients presenting at the clinics were personality disorders and depression.

[Early recognition centres for patients at risk of developing schizophrenia in Germany]. / Früherkennung und Frühbehandlung bei Patienten mit erhöhtem Schizophrenierisiko in Deutschland.

AIM OF THE STUDY: This survey gives a review over the development of early diagnosis and treatment of patients being at risk of developing psychoses in Germany. METHODS: A survey was carried out at 34 psychiatric departments at university hospitals in Germany from January until June 2008. RESULTS: So far, 12 early detection centres have been set up in Germany offering outpatient diagnostic and intervention services. CONCLUSIONS: Early recognition and intervention of psychoses has greatly improved in Germany in the last ten years. Therefore more research is imperative.

Effect of COMT val158met genotype on cognition and personality.

The gene encoding catechol-O-methyltransferase (COMT), an enzyme which regulates prefrontal cortex dopamine, contains a common functional single nucleotide polymorphism (val158met, rs4680G/A), which accounts for part of the interindividual variance in performance during working memory tasks and also predicts personality traits. We examined the relationship between the val158met polymorphism and cognitive function as well as personality traits in 522 healthy individuals (mean age: 24.75 years, SD=5.84, mean years of education: 15.59, SD=2.65). COMT val158met genotype was related in allele dosage fashion to performance in an executive function test, with the met/met carriers scoring highest. Subjects carrying the met/met genotype also scored higher in the disorganization domain of the SPQ-B personality inventory. Consistent with evidence from previous studies, higher dopamine availability of the met/met genotype enhances prefrontally mediated executive function in healthy individuals. Furthermore, we replicated findings from a recent study whereby the COMT genotype also predicts disorganized personality features.

The effect of body temperature on myocardial protection conferred by ischaemic preconditioning or the selective adenosine A1 receptor agonist GR79236, in an anaesthetized rabbit model of myocardial ischaemia and reperfusion.

1 The cardioprotective effect of N-[(1S, trans)-2-hydroxycyclopentyl]adenosine (GR79236), an adenosine A1 receptor agonist, was compared with that produced by ischaemic preconditioning in an anaesthetized rabbit model of myocardial ischaemia and reperfusion. In addition, we examined the effect of different body core temperatures on GR79236- or ischaemic preconditioning-induced cardioprotection when administered prior to ischaemia, and on cardioprotection induced by GR79236 administered 10 min prior to the onset of reperfusion. 2 When rabbits were subjected to 30 min occlusion of the left coronary artery, followed by 2 h reperfusion, GR79236 (3 x 10(-8) mol kg-1 i.v. (10.5 microg kg-1 i.v.)) or ischaemic preconditioning (5 min ischaemia followed by 5 min reperfusion), administered or applied 10 min prior to the occlusion, significantly limited the development of infarction. The cardioprotective effect of ischaemic preconditioning was significantly greater than that seen after administration of GR79236. Pre-treatment with the selective adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 3.3 x 10(-6) mol kg-1 (1 mg kg-1 i.v.)), prevented the cardioprotective effect of GR79236, but not that of ischaemic preconditioning. 3 Maintaining body core temperature at 38.5 degrees C rather than at 37.0 degrees C did not influence infarct size in control groups of rabbits, but reduced the cardioprotective effect of GR79236 when administered 10 min prior to occlusion or 10 min prior to the onset of reperfusion. The cardioprotective effect of ischaemic preconditioning was not temperature-dependent. 4 In conclusion, myocardial protection conferred by GR79236 in anaesthetized rabbits is mediated via adenosine A1 receptors. Myocardial protection can be conferred when GR79236 is administered before the onset of ischaemia or reperfusion, and is reduced when body core temperature is maintained at 38.5 degrees C rather than at 37.0 degrees C. In contrast, myocardial protection conferred by ischaemic preconditioning is not reduced by adenosine A1 receptor blockade, or by maintaining body core temperature at 38.5 degrees C rather than at 37.0 degrees C. These findings point to distinct differences in the mechanisms of induction of myocardial protection by adenosine A1 receptor agonist and ischaemic preconditioning. They also highlight the need for careful control of body core temperature when investigating the phenomenon of cardioprotection.