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Predominant polarity in bipolar disorder and validation of the polarity index in a German sample
(2014)
Background: A large number of patients with bipolar disorder (BD) can be characterized by predominant polarity (PP), which has important implications for relapse prevention. Recently, Popovic et al. (EUR NEUROPSYCHOPHARM 22(5): 339–346, 2012) proposed the Polarity Index (PI) as a helpful tool in the maintenance treatment of BD. As a numeric expression, it reflects the efficacy of drugs used in treatment of BD. In the present retrospective study, we aimed to validate this Index in a large and well characterized German bipolar sample.
Methods: We investigated 336 bipolar patients (BP) according to their PP and calculated the PI for each patient in order to prove if maintenance treatment differs according to their PP. Furthermore, we analysed whether PP is associated with demographic and clinical characteristics of BP.
Results: In our sample, 63.9% of patients fulfilled criteria of PP: 169 patients were classified as depressive predominant polarity (DPP), 46 patients as manic predominant polarity (MPP). The two groups differed significantly in their drug regime: Patients with DPP were more often medicated with lamotrigine and antidepressants, patients with MPP were more often treated with lithium, valproate, carbamazepine and first generation antipsychotics.
However, patients with DPP and MPP did not differ significantly with respect to the PI, although they received evidence-based and guideline-driven treatment.
Conclusion: The reason for this negative finding might well be that for several drugs, which were used frequently, no PI value is available. Nevertheless we suggest PP as an important concept in the planning of BD maintenance treatment.
Skin cytokine expression in patients with fibromyalgia syndrome is not different from controls
(2014)
Background
Fibromyalgia syndrome (FMS) is a chronic pain syndrome of unknown etiology. There is increasing evidence for small nerve fiber impairment in a subgroup of patients with FMS. We investigated whether skin cytokine and delta opioid receptor (DOR) gene expression in FMS patients differs from controls as one potential contributor to small nerve fiber sensitization.
Methods
We investigated skin punch biopsies of 25 FMS patients, ten patients with monopolar depression but no pain, and 35 healthy controls. Biopsies were obtained from the lateral upper thigh and lower calf. Gene expression of the pro-inflammatory cytokines tumor necrosis factor-alpha (TNF), interleukin (IL)-6, and IL-8 and of the anti-inflammatory cytokine IL-10 was analyzed using quantitative real-time PCR and normalizing data to 18sRNA as housekeeping gene. Additionally, we assessed DOR gene expression.
Results
All cytokines and DOR were detectable in skin samples of FMS patients, patients with depression, and healthy controls without intergroup difference. Also, gene expression was not different in skin of the upper and lower leg within and between the groups and in FMS patient subgroups.
Conclusions
Skin cytokine and DOR gene expression does not differ between patients with FMS and controls. Our results do not support a role of the investigated cytokines in sensitization of peripheral nerve fibers as a potential mechanism of small fiber pathology in FMS.
Impact of the AHI1 Gene on the Vulnerability to Schizophrenia: A Case-Control Association Study
(2010)
Background: The Abelson helper integration-1 (AHI1) gene is required for both cerebellar and cortical development in humans. While the accelerated evolution of AHI1 in the human lineage indicates a role in cognitive (dys)function, a linkage scan in large pedigrees identified AHI1 as a positional candidate for schizophrenia. To further investigate the contribution of AHI1 to the susceptibility of schizophrenia, we evaluated the effect of AHI1 variation on the vulnerability to psychosis in two samples from Spain and Germany. Methodology/Principal Findings: 29 single-nucleotide polymorphisms (SNPs) located in a genomic region including the AHI1 gene were genotyped in two samples from Spain (280 patients with psychotic disorders; 348 controls) and Germany (247 patients with schizophrenic disorders; 360 controls). Allelic, genotypic and haplotype frequencies were compared between cases and controls in both samples separately, as well as in the combined sample. The effect of genotype on several psychopathological measures (BPRS, KGV, PANSS) assessed in a Spanish subsample was also evaluated. We found several significant associations in the Spanish sample. Particularly, rs7750586 and rs911507, both located upstream of the AHI1 coding region, were found to be associated with schizophrenia in the analysis of genotypic (p = 0.0033, and 0.031,respectively) and allelic frequencies (p = 0.001 in both cases). Moreover, several other risk and protective haplotypes were detected (0.006,p,0.036). Joint analysis also supported the association of rs7750586 and rs911507 with the risk for schizophrenia. The analysis of clinical measures also revealed an effect on symptom severity (minimum P value = 0.0037). Conclusions/Significance: Our data support, in agreement with previous reports, an effect of AHI1 variation on the susceptibility to schizophrenia in central and southern European populations.
Der gasförmige Neurotransmitter Stickstoffmonoxid (NO) spielt eine Rolle bei verschiedenen physiologischen Vorgängen, aber auch psychiatrischen Erkrankungen wie Aggression, Ängstlichkeit, Depression und auch bei kognitiven Funktionen. Um mehr über die physiologische Rolle von NO herauszufinden untersuchten wir mittels Gen-Expressionsanalyse und Verhaltensversuchen Mäuse, bei denen die neuronale Isoform der Stickstoffmonoxidsynthase ausgeschaltet wurde. Die so genannte NOS-I ist die hauptsächliche Quelle von NO im zentralen Nervensystem. Knockout Tiere sind wertvolle Werkzeuge um sowohl den Einfluss eines Gens auf Verhalten als auch möglicherweise damit zusammenhängende Veränderungen des Transkriptoms zu identifizieren. Dies ist wichtig um herauszufinden, mit welchen molekularen Pfaden bestimmte Verhaltensweisen korreliert sind. In Bezug auf NOS-I gibt es zwei bisher beschriebene Knockout Mäuse Stämme. Es existieren KOex6 Knockout Mäuse, in welchen es überhaupt keine katalytisch aktive NOS-I gibt und es gibt einen Mausstamm, bei dem Exon 1 deletiert wurde, was aufgrund alternativer NOS-I Splicevarianten zu einer residualen Expression von bis zu 7% führt. Daher sind diese Mäsue besser zutreffend als Knockdown Mäuse zu bezeichnen. In der vorliegenden Arbeit untersuchten wir die Nos1 Knockdown Mäuse, da die hier vorliegende Situation wohl ähnlicher zu der bei menschlicher genetischer Varianten ist, da eine komplette Disruption bisher noch nicht beim Menschen beschrieben wurde. Es gibt diverse Studien, welche den behaviouralen Phänotyp der Nos1 Knockdown Mäuse untersuchen, aber diese widersprechen sich zum Teil. Bei unserer Untersuchung legten wir den Schwerpunkt auf Verhaltenstests, welche spezifische Symptome des Aufmerksamkeitsdefizit-/Hyperaktivitätssyndrom (ADHS) aufdecken sollten. Wir führten den Elevated Plus Maze Test (EPM) und ein modifiziertes Lochbrett-Paradigma, die COGITAT-Box, durch. Um die den gefundenen Verhaltensänderungen zugrunde liegenden molekularen Mechanismen herauszufinden, suchten wir nach Unterschieden der Expression des Serotonin- (5HTT) und des Dopamintransporters (DAT) zwischen den Knockdown und den Wildtyp Mäusen. Wir hatten spekuliert, dass die Disruption der NOS-I zu einer modifizierten Expression des DAT oder des 5HTT geführt habe könnte wegen den bekannten engen Interaktionen zwischen dem nitrinergen und den monoaminergen Systemen. Wir fanden einen diskret anxiolytischen Phänotyp, da die Knockdown Mäuse eine längere Zeit auf dem offenen Arm des EPM verbrachten bzw. häufiger den offenen Arm betraten im Vergleich zu dem Wildtypen. Dies war nicht durch eine höhere lokomotorische Aktivität zu erklären. Auch beobachteten wir ein geschlechterunabhängiges kognitives Defizit im Arbeits- und Referenzgedächtnis in der COGITAT-Box. Überraschenderweise fanden wir keine signifikante Dysregulation der Monoamin-Transporter in der Expressionsanalyse mittels der quantitativen Real Time PCR. Dies war eher unerwartet, da vorherige Studien verschiedene Veränderungen im serotonergen und dopaminergen System bei den Nos1 Knockdown Mäusen gefunden hatten, wie z.B. einen verminderten Serotonin-Umsatz in frontalen Cortex und hypofunktionale 5 HT1A and 5HT1B Rezeptoren. Auch ist bekannt, dass NO direkt Monoamin-Transporter nitrosyliert. Zusammenfassend zeigen die Nos1 Knockdown Mäuse ein charakteristisches behaviourales Profil mit reduzierter Ängstlichkeit und Defiziten im Gedächtnis. Weitere Studien sollten folgen um zu klären, ob diese Mäuse als Tiermodell für z.B. die Alzheimer-Erkrankung oder das Aufmerksamkeitsdefizit-/Hyperaktivitätssyndrom dienen könnten und die weitere pathophysiologische Rolle des NO bei neuropsychiatrischen Erkrankungen herauszufinden.