Benzodiazepines are the most utilized anxiolytic and hypnotic drugs. The high consumption of benzodiazepines has been a concern due to reported side effects of long-term use and dependence. Portugal has the highest benzodiazepine utilization in Europe.

To analyze the change in general practitioners’ (GPs) benzodiazepine prescription pattern after an intervention period.

An educational session was delivered to a group of intervened GPs. The benzodiazepine prescription pattern of intervened group was compared to the pattern of a non-intervened matched group from the same region, and of another non-intervened matched group from a different region. The research time frame was 12 months before and after intervention. The analysis of the prescription trends used the defined daily dose (DDD) and defined daily dose per 1000 patients per day (DHD) methodology. The statistical methods consisted of segmented regression analysis.

There was a decrease in benzodiazepine prescription pattern of intervened GPs after intervention (P = 0.005). There was also a decrease in benzodiazepine prescription pattern for the non-intervened group from the same region (P = 0.037) and for the non-intervened group from a different region (P = 0.010). Concerning an analysis by gender, female gender prescribed a higher amount of benzodiazepines. The intervened female gender prescribers presented the highest decrease in prescription trend after intervention (P = 0.008).

Intervention was effective in reducing benzodiazepine prescription after intervention. It demonstrates that a single intervention has a positive impact on improving prescription trends. The replication of this intervention might be an opportunity for changing the worrying benzodiazepine utilization in Portugal.

The authors have not supplied their declaration of competing interest.

Parkinsonian motor signs are the most frequent of the genuine motor abnormalities present in drug-naïve patients with schizophrenia, and are also present in patients with a first-episode of psychosis (FEP).

To study whether there are differences in basal ganglia volumes depending on the presence of Parkinsonism in FEP.

Forty-six patients with a FEP were included in the study. Twenty-three controls were included to normalise patients’ brain volume data. Parkinsonism was assessed with the UKU scale. Brain volumes were obtained with MRI (1.5 Tesla Siemens Avanto). Reconstruction and volumetric segmentation was made with the Freesurfer© software (http://surfer.nmr.mgh.harvard.edu/). Patients were divided into two groups, considering the presence/absence of Parkinsonism (UKU total score cutoff point = 4). Patients have been treated with antipsychotics a mean of less than 2 months. There were not significant differences in the total exposure to antipsychotics between both groups. ANCOVAS were performed including gender as covariate.

Patients with Parkinsonism showed a trend towards significance to exhibit reduced volumes in the left caudate and right putamen (Fig. 1).

FEP patients who exhibit Parkinsonian signs tend to show reduced left caudate and right putamen volumes in the early phases of psychotic illness, after correcting by gender.

The authors have not supplied their declaration of competing interest.

To investigate how brain metabolites, especially glutamate and glutamate to glutamine ratio of pgACC modulate the neural response within these areas and how this affects their function during emotion facial expression matching task.

Seventy healthy volunteers underwent magnetic resonance spectroscopy (MRS) and task functional magnetic resonance imaging (fMRI) in 7 Tesla scanner. PgACC MRS data were obtained using STEAM sequence and analyzed using LCModel.

Angry, fearful, and happy facial expressions were presented in an affect-matching block where one of the two facial expressions presented matched the target facial expression. The control condition was form matching. Data were preprocessed and analyzed in SPM 8.

Glutamate to Creatine ratio measured in pgACC positively correlated with BOLD response in the right DLPFC during negative emotional perception (FWE = 0.05) Glutamate to glutamine ratio indicating on-off mechanisms in pgACC positively correlated with BOLD responses in FFA extending to cerebellum cluster (FWE < 0.05).

This study indicate that pgACC, baseline metabolism predicts neural response to emotional processing. We conclude that individuals with higher glutamate ratios, an excitatory neurotransmitter, in pgACC during rest might have a better coping mechanism to potential danger indicated by perception of angry or afraid faces.

The higher glutamate to glutamine ratio in pgACC indicates a higher turnover of excitatory metabolite glutamate. This mechanism is associated with higher emotional response in fusiform area and cerebellum suggesting higher visual attention towards negative emotions.

The authors have not supplied their declaration of competing interest.

Emerging evidences indicate that the alteration of interhemispheric functional coordination may be involved in the pathogenesis of major depressive disorder (MDD). In present study, we aim to explore the potential marker by using the voxel-mirrored homotopic connectivity (VMHC) approach, which may be contributing to predict the clinical prognosis in MDD.

Eighty-two MDD patients and 50 normal control (NC) subjects participated in this study. We divided the MDD group into unremitted and remitted group according to the reduction rate of Hamilton Rating Scale for Depression (HAMD) within 2 weeks.

The study detected significantly decreased VMHC in bilateral precuneus (pCu), inferior temporal gyrus (ITG) and increased VMHC in middle frontal gyrus (MFG) and caudate nucleus when compared remitted depression (RD) group to unremitted depression (URD) group. Meanwhile, when compared with NC group, the URD group presented reduced VMHC in bilateral cerebellum anterior lobe, thalamus and postcentral gyrus. Furthermore, the VHMC in media frontal gyrus, postcentral gyrus and precentral gyrus were significantly decreased in RD group. Correlation analysis suggested that reduced VMHC in bilateral pCu was negatively correlated with the baseline HAMD score of URD (r = −0.325, P = 0.041). Receiver operating characteristic (ROC) curve indicated that three regional VMHC changes could identify depressed patient with poorer treatment response: ITG [area under curve (AUC) = 0.699, P = 0.002, 95% CI = 0.586–0.812], MFG (AUC = 0.692, P = 0.003, 95% CI = 0.580–0.805), pCu (AUC = 0.714, P = 0.001, 95% CI = 0.603–0.825).

The current study combined with previous evidence indicates that the subdued intrinsic interhemispheric functional connectivity might represents a novel neural trait involved in the pathophysiology of MDD.

The authors have not supplied their declaration of competing interest.

31P MRS is a unique way of in vivo energy metabolism research. This method allowed revealing schizophrenia-induced disturbances of energy exchange in resting state [1]. We use 31P MRS in presence of visual stimulation that allows neuronal energy-consuming processes studying.

Revealing of stimulation effects on high-energy phosphates (PCr, ATP) in early-stage schizophrenia.

Discovery of energy processes contribution in schizophrenia pathogenesis.

Twelve right-handed 18–26 years old male patients with early-staged schizophrenia (F20, ICD-10) and 20 age-matched healthy right-handed controls. Spectra were acquired on Philips Achieva 3.0 T using Rapid Biomed 31P/1H birdcage coil and 2D ISIS pulse sequence. fMRI was used for accurate 2D slice positioning, spectroscopy voxels containing primary visual cortex (V1) were averaged (see Fig. 1). Two 31P spectra of V1 were obtained: firstly in resting state and then during 6 minutes of continuous stimulation by 6 Hz flashing checkerboard. Spectra were processed in jMRUI.

Excitation reduced PCr in the norm and had no effect on schizophrenia (see Fig. 2). No excitation-induced ATP changes in both groups were revealed.

Alteration in PCr behavior in this study witnesses for deviations in energy-consuming processes in schizophrenia. A new scheme of neuronal response to stimulation in schizophrenia is offered.

The authors have not supplied their declaration of competing interest.

The aim of the FP7-European funded project TRIMAGE is to create a trimodal, cost-effective imaging tool consisting of PET/MR/EEG to enable effective early diagnosis of schizophrenia.

In the scope of this project we are interested in the multimodal assessment of response inhibition. The loudness dependence of auditory evoked potential (LDAEP) is a suitable biomarker of inhibitory action in signal processing. Variations in response inhibition can have great impact on different aspects of life. Individuals with reduced capability of inhibitory control have a tendency to impulsive behavior. Studies showed that they have stronger LDAEP values. Patients with schizophrenia may exhibit alterations in the responsiveness to sensory stimuli. Thus, a reduced LDAEP was found in these patients. However, these deviances differed in clinical features of the disorder. Therefore, we would like to further elucidate the relationship between multimodal neuroimaging methods and dimensions of symptoms, observable behavior, personality traits and general psychopathological dysfunction.

A sample of 20 healthy controls and 20 patients with manifest schizophrenia will be examined with the LDAEP paradigm in a trimodal approach with customary imaging tools. PET measurements with the radiotracer [11C]-flumazenil will be used to assess the binding potentials of GABA-A receptors. MRS will provide data about GABA concentrations. Simultaneously recorded EEG-fMRI data will permit new insight in the relationship between LDAEP and impulsivity.

The project will use alternative approaches to psychiatric classification. Response inhibition in sensory processing will be investigated from different angles (biochemical, neurophysiological, and neuroanatomical) and combined with psychological characteristic values.

The authors have not supplied their declaration of competing interest.

The authors have not supplied their declaration of competing interest.

The existing literature on chronic pain points to the effects anxiety sensitivity, pain hypervigilance, and pain catastrophizing on pain-related fear; however, the nature of the relationships remains unclear. The three dispositional factors may affect one another in the prediction of pain adjustment outcomes. The addition of one disposition may increase the association between another disposition and outcomes, a consequence known as suppressor effects in statistical terms.

This study examined the possible statistical suppressor effects of anxiety sensitivity, pain hypervigilance and pain catastrophizing in predicting pain-related fear and adjustment outcomes (disability and depression).

Chinese patients with chronic musculoskeletal pain (n = 401) completed a battery of assessments on pain intensity, depression, anxiety sensitivity, pain vigilance, pain catastrophizing, and pain-related fear. Multiple regression analyses assessed the mediating/moderating role of pain hypervigilance. Structural equation modeling (SEM) was used to evaluate suppression effects.

Our results evidenced pain hypervigilance mediated the effects of anxiety sensitivity (Model 1: Sobel z = 4.86) and pain catastrophizing (Model 3: Sobel z = 5.08) on pain-related fear. Net suppression effect of pain catastrophizing on anxiety sensitivity was found in SEM where both anxiety sensitivity and pain catastrophizing were included in the same full model to predict disability (Model 9: CFI = 0.95) and depression (Model 10: CFI = 0.93) (all P < 0.001) (see Figs. 3 and 4, Figs. 1 and 2).

Our findings evidenced that pain hypervigilance mediated the relationship of two dispositional factors, pain catastrophic cognition and anxiety sensitivity, with pain-related fear. The net suppression effects of pain catastrophizing suggest that anxiety sensitivity enhanced the effect of pain catastrophic cognition on pain hypervigilance.

The authors have not supplied their declaration of competing interest.

Cluster B personality disorder (PD) is a highly prevalent mental health condition in general population (1 to 6% depending on the subtype and study). Patients affected are known to be heavier users of both mental and medical healthcare than other clinical conditions such as depression. Few studies have highlighted their elevated mortality rate compared to general population.

The estimates were produced using data from the integrated monitoring system for chronic disease of Quebec. It provides annual and life prevalence, mortality rate, years of and healthcare utilization profile Quebec inhabitants.

A total of 7,995,963 people were included in the study. The life prevalence of cluster B PD is 2.6%. The mean years of lost life is 13 for men and 9 for women when they are compared to general population. The 3 most important causes of death are: suicide (20.4%), cardiovascular diseases (19.1%) and cancers (18.6%). The standardized mortality ratio (SMR) for each medical condition is superior in cluster B personality disorders than general population. The most important SMR is for suicide (male: 10.2 and female: 21). In the year 2011–2012, 78% had consulted a general practitioner, 62% a psychiatrist, 41% were admitted in an emergency department and 21% were hospitalized.

The authors have not supplied their declaration of competing interest.

Both attachment style and personality traits are closely related to individual's interpersonal patterns. Association between these constructs has been widely studied, but variability in results makes it difficult to reach definite conclusions. Similarly, dopaminergic pathways are considered to underlie some personality traits and to be related to attachment styles, but evidence, hitherto, remain inconclusive.

To assess the correlation between personality and attachment dimensions and to study whether a common association to the catechol-O-methyltransferase (COMT) Val158Met polymorphism exists.

One hundred and three Caucasian controls (mean age 39.6 ± 6.4; 65% women) were recruited in the province of Biscay, Spain. DAPP-BQ and ECR-Spanish scales were administered to assess personality and attachment dimensions respectively. DNA was obtained from saliva and the COMT Val158Met polymorphism was determined. Pearson's correlation coefficient and ANOVA were calculated using R statistical software.

High positive correlation is observed between inhibition personality dimension and attachment avoidance (r = 0.75). Besides, both inhibition and avoidance dimensions’ scores are significantly higher in the COMT ValMet genotype than in the other genotypes. MetMet: 63.1 ± 13.6; ValMet: 71.0 ± 13.9; ValVal: 63.0 ± 16.7 (ANOVA F = 3.75, P = 0.027) for inhibition and MetMet: 3.44 ± 0.17; ValMet: 3.82 ± 0.2; ValVal: 3.33 ± 0.23 (ANOVA F = 3.83, P = 0.025) for avoidance.

Attachment patterns are rooted in early interactions with parental figures, and according to our results they could be linked to self-perceived personality traits in adulthood. Our study also suggests that genetics may predispose individuals to certain interaction styles. Our findings, linking ValMet individuals to avoidant attachment, are similar to Luijk's (2011) results, and would support a genetic-environmental model of both attachment and personality.

The authors have not supplied their declaration of competing interest.

A history of traumatic events is prevalent in people with schizophrenia spectrum disorders and mood disorders. However, little is known about their etiological relationship.

To explore whether patients with acute or posttraumatic stress disorder are at higher risk of developing a schizophrenia spectrum disorder or mood disorder.

In this prospective cohort study using registers covering the entire Danish population, we used the Danish Psychiatric Central Research Register to identify patients with ICD-10 diagnoses of acute traumatic stress disorder and/or posttraumatic stress disorder. From inpatient and outpatient mental hospitals, we identified 4371 diagnoses with more than 18 million years of follow-up. Main outcomes and measures were relative risks (RR) with 95% confidence intervals (95% CI) of schizophrenia, schizophrenia spectrum disorder, bipolar disorder and mood disorder.

The incidence of traumatic stress disorder (TSD) has increased steadily from 0.6% in 1996 to 6% in 2012, showed a higher incidence in women and an age distribution with a peak-incidence in early adulthood. We found that diagnoses of TSD increase the risk of schizophrenia (RR 5.85, 95% CI 3.59–8.91), schizophrenia spectrum disorder (RR 3.82, 95% CI 2.38–5.75), bipolar disorder (RR 5.83, 95% CI 3.11–9.83) and mood disorder (RR 4.10, 95% CI 3.15–5.22). Risks were high in the first year after diagnosis of TSD and declined going forward in time.

Our findings indicate that acute and posttraumatic stress disorder are etiological risk factors for schizophrenia spectrum disorders and mood disorders. If replicated, this may underline treatment of traumatized patients in prevention of severe mental disorder.

The authors have not supplied their declaration of competing interest.

Some inconsistent evidence indicates experiences of trauma and the presence of symptoms of PTSD are associated with increased risk of cardiovascular diseases. This relation has rarely been explored with community samples including participants with PTSD symptoms or who fulfill criteria for PTSD disorders.

We identify those with a high number of PTSD symptoms and those fulfilling criteria for PTSD are more likely to have CVD than those without a PTSD syndrome or diagnosis. We examine rates of mental health access for those with PTSD and CVD.

We use Collaborative Psychiatric Epidemiology Surveys (CPES) to examine differences in trauma/PTSD prevalence and the association of prior trauma exposure and PTSD diagnoses with CVD (n = 13,286). CIDI was used to make psychiatric diagnoses and medical data was acquired regarding onset and severity of CVD.

Individuals with prior exposure to trauma and PTSD diagnoses had twice the likelihood of developing a cardiovascular disease as those without trauma exposure [OR = 1.77, 95% CI (1.0, 2.94)]. Having a PTSD diagnosis is a significant predictor of having a CVD for individuals who experienced a traumatic event.

The probability of developing a CVD was higher when patients had prior diagnosis of substance abuse [OR = 1.36, 95% CI (1.11, 1.65)] or mental health disorders [OR = 1.43, 95% CI (1.10, 1.87) for depression; OR = 1.33, 95% CI (1.04, 1.69) for anxiety]. Men were almost twice as likely as women to be diagnosed with a CVD [OR = 1.67, 95% CI (1.37, 2.00)].

Exposure to trauma and the presence of PTSD symptoms are significantly associated with CVD.

The authors have not supplied their declaration of competing interest.

In cooperation with Joachim Cordes, Andreas Bechdolf, Christina Engelke, Kahl KG, Chakrapani Balijepalli, Christian Lösch, Joachim Klosterkötter, Michael Wagner, Wolfgang Maier, Andreas Heinz, Walter de Millas, Wolfgang Gaebel, Frank Schneider, Martin Lambert, Georg Juckel, Thomas Wobrock, Michael Riedel, Susanne Moebus.

In vitro studies have demonstrated possible neuroprotective effects of the following pro-inflammatory cytokines: IL-6, IL-1β and TNF-α against glutaminergic excitotoxicity in brain through different pathways.

In the current study, we aim to correlate level of the above pro-inflammatory cytokines in serum with glutamate levels in head of caudate nucleus measured using Proton Magnetic Resonance Spectroscopy (1H-MRS) in patients with obsessive-compulsive disorder (OCD), a neuropsychiatric illness with possible multifactorial aetiology including immunological and excitotoxic factors.

Thirty psychotropic-naïve patients with OCD and an equal number of gender and age-matched normal controls were recruited in the study. A detailed psychiatric assessment was carried out including sociodemographic and clinical variables. A 3T MR imaging and spectroscopy session was carried out in head of caudate nucleus. Further, absolute quantification of glutamate level was obtained using LC model. Simultaneously, 5 mL of blood sample was collected and assayed for the above pro-inflammatory cytokines (Siemens, Immulite™). The level of glutamate was correlated with the cytokine levels in patients with OCD.

The level of Glx was significantly higher in patients with OCD as compared to controls (P < 0.05). The Glx level negatively correlated with two of the three pro-inflammatory cytokines: IL-6 and TNF-α (r = −0.807; r = −0.838; P < 0.05) while no significant correlation was demonstrated with IL-1β.

The findings provide preliminary evidence regarding possible neuroprotective effects of pro-inflammatory cytokines against glutaminergic excitotoxicity in patients with OCD. Further studies including patients with other psychiatric illnesses as controls are required for confirmation of the above findings.

The authors have not supplied their declaration of competing interest.

A large number of studies have reported that the prolactin concentration was significantly increased in the Taq1A A1 allele carriers because several reports revealed that individuals with the DRD2 Taq1A A1 allele have a reduced density of brain D2 receptors.

The main aim of this study was to identify the impact of pharmacogenetic markers associated with prolactin concentration in risperidone-treated children and adolescents with autism spectrum disorders.

One hundred and forty-seven children and adolescents with autism, aged 3 to 19, received risperidone. The clinical data of patients were recorded from medical records. Prolactin levels were measured by chemiluminescence immunoassay. Three CYP2D6 single nucleotide polymorphisms (SNPs), CYP2D6*4 (1846G>A), *10 (100C>T), and *41 (2988G>A), one gene deletion (*5), and DRD2 Taq1A (rs1800497) polymorphism were genotyped by TaqMan real-time PCR.

The three common allelic frequencies were CYP2D6*10 (55.10%), *1 (32.65%) and *5 (6.12%), respectively. Patients were grouped according to their CYP2D6 genotypes. The DRD2 genotype frequencies were Taq1A A2A2 (38.77%), A1A2 (41.50%), and A1A1 (19.73%), respectively. There were statistically significant differences in prolactin level of patients among the three groups (P = 0.033). The median prolactin level in patients with DRD2 Taq1A A2A2 (17.80 ng/mL) was significantly higher than A1A2 (17.10 ng/mL) and A1A1 (12.70 ng/mL).

DRD2 Taq1A A2A2 polymorphisms may be a critical role in an influence prolactin elevation during risperidone treatment in ASD.

The authors have not supplied their declaration of competing interest.

The determination of the accurate CYP2D6 genotyping is essential in the clinical setting and individualization of drug therapy.

In this study, was to apply the Luminex xTAG technology to detect significant CYP2D6 polymorphisms and copy number variation, including assessment the relationship of CYP2D6 polymorphisms and risperidone plasma concentration in autism spectrum disorder children (ASD) treated with risperidone.

All 84 ASD patients included in this study had been receiving risperidone at least for 1 month. The CYP2D6 genotypes were determined by luminex assay. Plasma concentrations of risperidone and 9-hydroxyrisperidone were measured using LC/MS/MS.

Among the 84 patients, the most common genotype was CYP2D6*1/*10 (26.19%). The most common allele was CYP2D6*10 (51.79%) and the second most allele was CYP2D6*1 (27.98%). There were 46 (55.42%) classified as EM, 33 (39.76%) as IM, and 4 (4.82%) as UM. The plasma concentration of risperidone and risperidone/9-hydroxyrisperidone ratio in the patients were significant differences among the CYP2D6 predicted phenotype group (P = 0.001 and P < 0.0001, respectively). Moreover, the plasma concentration of risperidone and risperidone/9-hydroxyrisperidone ratio in the patients with CYP2D6 activity score 0.5 were significantly higher than those with the CYP2D6 activity score 2.0 (P = 0.004 and P = 0.002, respectively).

The present study suggests that it would be ideal to identify the CYP2D6 genotype of patients before prescribing and administering risperidone. Furthermore, the use of CYP2D6 gene scoring system to determine an individual's metabolic capacity may become an essential tool for a more rational and safer drug administration.

The authors have not supplied their declaration of competing interest.

A critical need exists for progress in the characterization of targets for pro-cognitive drug discovery. We previously demonstrated that Telmisartan (TLM), an angiotensin type 1 receptor (AT1) blocker and partial agonist of peroxisome proliferator-activated receptor gamma (PPARγ), alleviates cognitive decline in chronically stressed rats. Understanding of mechanistic background of this phenomenon is hampered by both dual binding sites of TLM and limited data on the molecular consequences of central AT1 blockade and PPARγ activation.

To discriminate molecular effects of AT1 blockade and PPARγ activation in stress induced memory impairment.

In this study, we investigated mechanism of neuroprotection provided by TLM in chronic psychological stress.

We analyzed BDNF gene expression in the hippocampus (HIP) and medial prefrontal cortex (mPFC) in chronically restrained stressed Wistar rats (2.5 h, 21 days), repeatedly treated with TLM (1 mg/kg), GW9662 (0.5 mg/kg) – a selective PPARγ receptor antagonist, or both in combination. TATA box binding protein (Tbp) was an internal control for expression studies.

Alterations of mRNA expression of BDNF are shown on Figs. 1 and 2.

AT1 receptor blockade restores cognitive functions in chronically stressed subjects, which is associated with changes in primarily cortical gene expression.

The authors have not supplied their declaration of competing interest.

The pattern of changes can be related with the differences between perioperative expectations and real long-term outcomes. Correlations between changes seen in BDI and SF36 scores with age can be considered as a confirmatory evidence for this idea.

All cases showed an insignificant gradual decline in digit span test, which may be independent of the surgical procedure. Although the COWA test could not prove a significant deterioration in verbal fluency but a slight decline after one year was obvious, in addition to one patient who turned aphasic during this period.

The outcomes showed that the benefits of DBS outweigh the slight risk of developing depression.

The authors have not supplied their declaration of competing interest.

MDD is a common, chronic and recurrent illness .it is essential to reach full remission in acute treatment. tDCS is a non-invasive brain stimulation that uses direct electrical currents to stimulate specific parts of the brain.

Is to assess the effectiveness of tDCS in patients with treatment resistance MDD.

Eighty outpatients of a psychiatric clinic were selected. Subjects meet (DSM-IV) diagnostic criteria for MDD. All patients had failed to respond to at least two standard antidepressant medication, in the current episode. Patients with bipolar depressive disorder, MDD with psychotic and atypical features, other psychiatric disorders, sever medical condition, acute suicidality and pregnancy were excluded. All patients received stable drug regimens for at least two weeks before enrollment and drug dosages remained unchanged throughout the study. They revised 8 stimulation sessions, using a 2 mA current, for 20 minutes, in 8 consecutive days. The anodal electrode was placed over the left DLPFC. Cathode electrode over the right supraorbital region. Mood was evaluated with 21-item Hamilton Rating Depression Scale and the Beck Depression Inventory.

We designed a pretest–posttest study and evaluate depression at baseline (pre-intervention), immediately after 8 sessions (post-intervention) and two months after treatment onset (follow-up).

There is a significant difference between Pre- vs. post-intervention (FBDI = 246.58, P < 0.001; FHRSD = 214.56, P < 0.001) and pre vs. Follow-up intervention (FBDI = 323.10, P < 0.001; FHRSD = 150.96, P < 0.001).

It can be said that tDCS had effective and enduring variation (P post vs. follow-up > 0.05) in improving the clinical symptoms of MDD.

The authors have not supplied their declaration of competing interest.

Limitations of available treatment methods of dementia imply constant need to search for new, supplementary therapy strategies. There is a consensus that vascular lesions, oxidative stress, inflammatory processes and abnormal neurotransmission are associated with dementia. Due to the anti-inflammatory (modification of pro-inflammatory cytokines concentration), antioxidative effect of cryogenic temperatures as well as the hormonal and lipid changes, they may play an important role in preventing or inhibiting pathophysiological processes.

To assess the influence of whole-body cryostimulation on cognitive functions of patients with MCI.

RCT design is used to examine the influence of whole-body cryotherapy (WBC) on people with mild cognitive impairments (MCI) with the evaluation of psychometric, somatic and laboratory parameters. Participants undergo 10 sessions each day of 2–3 min of WBC in experimental group (−110 till −160 °C) and placebo (−20 °C). The CDR, MoCA, TYM, DemTect and SLUMS scales are used among others at baseline and follow-up. Preliminary data of 7 volunteers (n = 7, 49–79 years old) were presented. Results on Fig. 1.

Among obtained psychometric results show that all, except of one, patients significantly improved their scores after WBC. That is a very promising feedback for future evaluation of WBC effectiveness in prevention of dementia in patients with MCI.

The authors have not supplied their declaration of competing interest.