A prominent theory of depression focusses on neural plasticity and stress as central issues in seeking to develop a pattern of identifiable biological markers for the depressive disorders. Relative neglect, however, of clinical factors in that theory limits the uncovering of markers and opens to question their methodological approach. A conflicting theory, the ‘opposed neurobehavioral states’, based on dimensional analysis of monoamine neurotransmitter systems and behavioural factors is presented. This perspectives paper contrasts the two approaches viewing the biomarkers theory as premature at this point in the progress of depression research.

Studies developed to support the biomarkers theory and the opposed neurobehavioral states theory are examined for their strengths and limitations in explaining the nature of the disorder and the actions of therapeutic drugs. Reference is made to reviews of the many studies on biomarkers and the recent work that supports the opposed neurobehavioral states theory.

Main issue: the biomarkers theory sets important goals, but despite the many advances in the neural investigations of factors underlying depression, is still not successful in specifying markers. Thus, it is believed to be applying the wrong methodologic approach and premature in its claims. Perspective: the ‘opposed neurobehavioral’ theory is limited in its breadth of research. It applies, however, the dimensional approach to the clinical side of the problem, a methodological approach more likely to be effective in selecting the best clinical treatment and open to a more productive path to understanding of the nature of the disorder in future research.

The aim of this study was to evaluate the dynamic thiol–disulphide homeostasis as an oxidative stress parameter, using a newly proposed method, in patients with Alzheimer’s disease.

In total, 97 participants were included in the study. Among them, 51 had been diagnosed with Alzheimer’s disease, and the remaining 46 were healthy individuals. Total thiol (–SH+–S–S–) levels and native thiol (–SH) levels in serum of each participant were measured. The amount of dynamic disulphide bonds (–S–S–) and (–S–S–) ×100/(–SH), (–S–S–) ×100/(–SH+–S–S–), and –SH×100/(–SH+–S–S–) ratios were calculated from these values. The obtained data were used to compare Alzheimer’s disease patients with healthy individuals.

The average total thiol and native thiol levels of patient with Alzheimer’s disease in the study were found to be significantly lower than those levels of healthy individuals. In addition, in the patient group, the –S–S–×100/–S–S+–SH ratio was found to be significantly higher, whereas the –SH×100/–S–S+–SH ratio was found to be significantly lower compared with healthy individuals. Total thiol and native thiol levels, dynamic disulphide bond amount, and –S–S–×100/–SH, –S–S–×100/–S–S+–SH, and –SH×100/–S–S+–SH ratios were not found to be correlated with mini mental state examination score or duration of disease.

Recent studies have shown that oxidative stress is the one of the molecular changes underlying the pathogenesis of Alzheimer’s disease. In this study, we have investigated the dynamic thiol–disulphide homeostasis in patients with Alzheimer’s disease, using a novel method.

For centuries, cannabinoids have been known to be effective in pain states. Itch and pain are two sensations sharing a lot in common.

The goal of this research was to observe whether the cannabinoid agonist WIN 55,212-2 reduces serotonin-induced scratching behaviour and whether neurotoxic destruction of descending serotonergic and noradrenergic pathways mediate the antipruritic effect of WIN 55,212-2.

Scratching behaviour was induced by intradermal injection of serotonin (50 µg/50 µl/mouse) to Balb/c mice. The neurotoxins 5,7-dihydroxytryptamine (5,7-DHT, 50 μg/mouse) and 6-hydroxydopamine (6-OHDA, 20 μg/mouse) are applied intrathecally to deplete serotonin and noradrenaline in the spinal cord. WIN 55,212-2 (1, 3, 10 mg/kg, i.p.) dose-dependently attenuated serotonin-induced scratches. Neurotoxic destruction of neither the serotonergic nor the noradrenergic systems by 5,7-DHT and 6-OHDA, respectively, had any effect on the antipruritic action of WIN 55,212-2.

Our findings indicate that cannabinoids dose-dependently reduce serotonin-induced scratching behaviour and neurotoxic destruction of descending inhibitory pathways does not mediate this antipruritic effect.

Asenapine is an atypical antipsychotic that is currently available for the treatment of schizophrenia and bipolar I disorder. Although the atypical antipsychotics clozapine and olanzapine are effective for depression and anxiety in schizophrenia, as demonstrated by animal model studies, this has not been clarified for asenapine. Therefore, we compared the effects of asenapine in the conditioned fear stress model with those of clozapine and olanzapine.

Rats were individually fear conditioned using electrical foot shock in a Skinner box. Approximately 24 h later, individual animals were returned to the same Skinner box (without electrical shock) and their freezing behaviour was observed for 5 min. Animals were treated with asenapine, clozapine, olanzapine, the 5-HT1A receptor partial agonist buspirone, or the 5-HT2C receptor antagonist SB242084 at 30 min before freezing behaviour assessment. The 5-HT1A receptor antagonist WAY100635 or the 5-HT2C receptor agonist Ro60-0175 was also used concomitantly with asenapine. The effects of asenapine, clozapine, and olanzapine on serotonin release in the rat hippocampus were also measured using in vivo microdialysis.

Asenapine reduced freezing behaviour, while neither clozapine nor olanzapine reduced freezing behaviour. Buspirone and SB242084 also reduced freezing behaviour. The effect of asenapine in reducing freezing behaviour was not altered by the concomitant administration of WAY100635 or Ro60-0175. Both asenapine and clozapine, but not olanzapine, increased serotonin release in the rat hippocampus.

Asenapine may have superior therapeutic effect on anxiety symptoms than other agents, although the underlying mechanism of its anxiolytic activity remains unknown.

Using data from the Research on Asian Psychotropic Prescription Patterns for Antidepressants (REAP-AD) study, we aimed to present the rates and clinical correlates of suicidal thoughts/acts in patients recruited from a total of 40 centres in 10 Asian countries/areas: China, Hong Kong, India, Indonesia, Japan, Korea, Malaysia, Singapore, Taiwan, and Thailand.

Data from 1122 patients with depressive disorders in the REAP-AD study were used. The ICD-10 was employed to diagnose depressive episodes and recurrent depressive disorder. The presence or absence of suicidal thoughts/acts and profile of other depressive symptoms was established using the National Institute for Health and Clinical Excellence guidelines for depression. Country/area differences in rates of suicidal thoughts/acts were evaluated with the χ2 test. In addition, depressive symptom profiles, other clinical characteristics, and patterns of psychotropic drug prescription in depressed patients with and without suicidal thoughts/acts were compared using analysis of covariance for continuous variables and logistic regression analysis for discrete variables to adjust the effects of covariates.

The rates of suicidal thoughts/acts in 10 countries/areas varied from 12.8% in Japan to 36.3% in China. Patients with suicidal thoughts/acts presented more persistent sadness (adjusted odds ratio [aOR]=2.64, p<0.001), loss of interest (aOR=2.33, p<0.001), fatigue (aOR=1.58, p<0.001), insomnia (aOR=1.74, p<0.001), poor concentration (aOR=1.88, p<0.001), low self-confidence (aOR=1.78, p<0.001), poor appetite (aOR=2.27, p<0.001), guilt/self-blame (aOR=3.03, p<0.001), and use of mood stabilisers (aOR=1.79, p<0.001) than those without suicidal thoughts/acts.

Suicidal thoughts/acts can indicate greater severity of depression, and are associated with a poorer response to antidepressants and increased burden of illness. Hence, suicidal thoughts/acts can provide a clinical index reflecting the clinical status of depressive disorders in Asians.

To assess the relationship between states of anger and stroke.

Systematic review of the literature.

In total, 21 papers were selected for the systematic review of data published on the subject of anger and stroke. A state of anger may be a risk factor for stroke, as well as a consequence of brain lesions affecting specific areas that are caused by a stroke. Scales to assess anger varied among authors. There was no consensus regarding the area of brain lesions that might lead to a state of anger. Although some authors agreed that lesions on the right side led to angrier behaviour, others found that lesions on the left side were more relevant to anger. Likewise, there was no consensus regarding the prevalence of anger pre or post-stroke. Some authors did not even find that these two conditions were related.

Although most authors have accepted that there is a relationship between anger and stroke, studies with uniform methodology need to be conducted if this association is to be properly evaluated and understood.

Neuroimaging studies of depression considered as a stress-related disorder have shown uncoupling in regional cerebral blood flow (rCBF) and regional cerebral metabolic rate for glucose (rCMRglc). We hypothesised that the mismatch change of rCBF and rCMRglc could be a stress-related phenomenon.

We exposed male rats to 15-min period of forced swim (FS), followed by the measurement of rCBF using N-isopropyl-4-[123I] iodoamphetamine (123I-IMP) and rCMRglc using 2-deoxy-2-[18F] fluoro-D-glucose (18F-FDG).

The uptake rate of 18F-FDG in the FS group showed a significant decrease in the prefrontal cortex (0.86±0.20%ID/g, p<0.01) and thalamus (0.77±0.17%ID/g, p<0.05) and tended to be lower in the hippocampus (0.58±0.13%ID/g) and cerebellum (0.59±0.13%ID/g) without overt alteration in the uptake rate of 123I-IMP.

The FS stress can cause mismatch change of rCBF and rCMRglc, which reflect a stress-related phenomenon.

Immune system activation is involved in the pathophysiology of panic disorder (PD). We investigated INF-γ+874 A/T, TNF-α-308 G/A, and IL-10-1082 G/A single nucleotide polymorphisms (SNPs) to determine their association with PD.

This study enroled 135 PD patients and 135 healthy controls. INF-γ+874 A/T (rs2430561), TNF-α-308 G/A (rs1800629), and IL-10-1082 G/A (rs1800896) were genotyped.

There were no differences in genotypes or allele frequencies between the patient and control groups, regardless of accompanying agoraphobia. However, for female patients, the G allele frequency in IL-10 SNP was higher in the control group than in the patient group. Additionally, the female control group had a higher frequency of the A/G and G/G genotype in the IL-10 SNP than the female patient group.

We suggest that the G allele in IL-10-1082 G/A might have a role in reducing the manifestations of PD in female patients. Further studies are needed to extend and confirm our findings.

After the prevalence of syphilis had reached historic lows, the Center for Disease Control devised a plan to eradicate syphilis in the United States. Since that decree there has been a dramatic rise in new cases. Psychosis is an ominous symptom of neurosyphilis.

We report a case of neurosyphilis that was misdiagnosed and staged incorrectly.

Failure to diagnose neurosyphilis was associated with prolonged psychosis that has been refractory to antipsychotic treatment.

Psychiatrists should renew their vigilance for neurosyphilis in the setting of a positive screening test and psychosis.