The present study was designed to test the hypothesis that there is a reduction in the activity of the enzyme cytochrome c oxidase (Cox) in Alzheimer’s disease (AD).

Systematic review of literature and meta-analysis were used with data obtained from the PubMed, Scopus, MEDLINE, Lilacs, Eric and Cochrane. The keywords were Alzheimer’s AND Cox AND mitochondria; Alzheimer’s AND Cox AND mitochondria; Alzheimer’s AND complex IV AND mitochondria. A total of 1372 articles were found, 23 of them fitting the inclusion criteria. The data were assembled in an Excel spreadsheet and analysed using the RevMan software. A random effects model was adopted to the estimative of the effect.

The data shows a significant decrease in the activity of the Cox AD patients and animal models.

Cox enzyme may be an important molecular component involved in the mechanisms underlying AD. Therefore, this enzyme may represent a possible new biomarker for the disease as a complementary diagnosis and a new treatment target for AD.

The aim of this study was to identify factors associated with acceptability and efficacy of yoga training (YT) for improving cognitive dysfunction in individuals with schizophrenia (SZ).

We analysed data from two published clinical trials of YT for cognitive dysfunction among Indians with SZ: (1) a 21-day randomised controlled trial (RCT, N = 286), 3 and 6 months follow-up and (2) a 21-day open trial (n = 62). Multivariate analyses were conducted to examine the association of baseline characteristics (age, sex, socio-economic status, educational status, duration, and severity of illness) with improvement in cognition (i.e. attention and face memory) following YT. Factors associated with acceptability were identified by comparing baseline demographic variables between screened and enrolled participants as well as completers versus non-completers.

Enrolled participants were younger than screened persons who declined participation (t = 2.952, p = 0.003). No other characteristics were associated with study enrollment or completion. Regarding efficacy, schooling duration was nominally associated with greater and sustained cognitive improvement on a measure of facial memory. No other baseline characteristics were associated with efficacy of YT in the open trial, the RCT, or the combined samples (n = 148).

YT is acceptable even among younger individuals with SZ. It also enhances specific cognitive functions, regardless of individual differences in selected psychosocial characteristics. Thus, yoga could be incorporated as adjunctive therapy for patients with SZ. Importantly, our results suggest cognitive dysfunction is remediable in persons with SZ across the age spectrum.

Vitamin D deficiency may be a clinical problem in patients with addictions. The authors systematically searched for studies addressing vitamin D and addiction and develop a hypothesis which can direct future research of the possible mechanistic role of vitamin D in the process of addiction.

Systematic review of the literature found in PubMed and EMBASE followed by narrative review combined with clinical experiences leading to hypotheses for future research.

Only five articles were identified about a role of vitamin D in the pathophysiology of addiction. Their results are in line with a possible influence of vitamin D in dopaminergic transmission. The cerebral vitamin D status depends on the functionality of genetic variants of vitamin D receptor and other involved genes. Routine serum calcidiol levels may not adequately reflect cerebral vitamin D status. Uncertainty exists regarding appropriate calcidiol blood levels and proper dosages for affecting the central nervous system (CNS).

The putative pathophysiological role of vitamin D in substance abuse has been insufficiently studied which calls to more studies how to measure cerebral vitamin D status in clinical practice. Research is indicated whether vitamin D supplementation should use higher dosages and aim to reach higher calcidiol serum levels. Measuring dopaminergic functioning within the prefrontal cortex as reflected by neuropsychological tests selected as suitable could be a appropriate proxy for the cerebral vitamin D status when studying the pharmacogenomics of this functionality in patients.

Previous studies have examined the effect of transcranial direct current stimulation (tDCS) on the in-vivo concentrations of neuro-metabolites assessed through magnetic resonance spectroscopy (MRS) in neurological and psychiatry disorders. This review aims to systematically evaluate the data on the effect of tDCS on MRS findings and thereby attempt to understand the potential mechanism of tDCS on neuro-metabolites.

The relevant literature was obtained through PubMed and cross-reference (search till June 2020). Thirty-four studies were reviewed, of which 22 reported results from healthy controls and 12 were from patients with neurological and psychiatric disorders.

The evidence converges to highlight that tDCS modulates the neuro-metabolite levels at the site of stimulation, which, in turn, translates into alterations in the behavioural outcome. It also shows that the baseline level of these neuro-metabolites can, to a certain extent, predict the outcome after tDCS. However, even though tDCS has shown promising effects in alleviating symptoms of various psychiatric disorders, there are limited studies that have reported the effect of tDCS on neuro-metabolite levels.

There is a compelling need for more systematic studies examining patients with psychiatric/neurological disorders with larger samples and harmonised tDCS protocols. More studies will potentially help us to understand the tDCS mechanism of action pertinent to neuro-metabolite levels modulation. Further, studies should be conducted in psychiatric patients to understand the neurological changes in this population and potentially unravel the neuro-metabolite × tDCS interaction effect that can be translated into individualised treatment.

The COVID-19 pandemic has drastically changed society and introduced many new factors to consider in adolescent suicide risk assessment and prevention. One complexity that warrants consideration is the male-specific impacts of the pandemic within adolescence.

A review of the relevant literature.

Matters of social distancing, virtual education, and substance use may impact adolescent men in fashions that raise their suicide risk more significantly relative to adolescent women. Social distancing may impact adolescents’ friendships and generate a regression back to the nuclear family; qualities of male adolescents’ friendships and of masculinity suggest that these impacts may be more severe in adolescent men and may directly raise suicide risk. Virtual schooling yields educational and social setbacks; losses of team sports, male mentors, and the implications of diminished educational advancement may more adversely affect adolescent men and raise risk. Substance use has increased in the pandemic, particularly amongst adolescent men. There are direct associations with suicide risk as well as indirectly through increased parental conflict and punishment.

As adolescent men die by suicide at significantly elevated rates relative to adolescent women, a male-specific consideration of these impacts is indicated to address adolescent suicide in our current era. Recommendations are made for integrating these considerations into updated adolescent suicide risk assessment and prevention efforts.

To assess the prevalence of mood disorders in Brazilian soldiers.

A total of 353 soldiers answered the following questionnaires: the Beck Depression Inventory (BDI), the State-Trait Anxiety Inventory (STAI), the Profile of Mood States (POMS), the medical outcomes study SF-36 questionnaire, the Baecke questionnaire to assess the level of habitual physical activity (HPA) and the socioeconomic (SE) status questionnaire. Participants were classified according to their desire to pursue a military career.

Accordingly, 246 participants were allocated to a volunteer group (VG) and 107 to a non-volunteer group (NVG). According to the BDI data for both groups, 66.5% of the soldiers showed at least mild depressive symptoms. Additionally, the STAI data revealed that 27.8% and 8.4% of the soldiers showed high scores on state anxiety and trait anxiety, respectively. The POMS scores were higher in the NVG compared to the VG (Δ%=+263%, p<0.0001). Of the eight subscales, the SF-36 questionnaire showed statistical differences between the groups in the following five dimensions: functioning capacity (p = 0.0046), pain (p = 0.0011), vitality (p < 0.0001), role limitations due to emotional problems (p < 0.0001) and mental health (p < 0.0001).

Mood disorder levels were higher and health status and related quality of life levels were lower in the NVG as compared to the VG.

Bipolar disorder (BD) may be connected with accelerated aging, the marker of this can be shorter telomere length (TL). Some data suggest that lithium may exert a protective effect against telomere shortening. The study aimed to compare the TL between patients with BD and control subjects. The effect of long-term lithium treatment was also assessed.

The study group comprised 41 patients with BD, including 29 patients treated longitudinally with lithium (mean 16.5 years) and 20 healthy people. TL was assessed by the quantitative polymerase chain reaction (qPCR).

In the control group, the TL was significantly longer in males than in females. Male bipolar patients had significantly shorter TL compared with the control male group. In bipolar patients, there was no correlation between TL and duration of treatment. The TL was negatively correlated with age in male bipolar patients.

The study did not confirm the lithium effect on TL in bipolar patients. TL showed gender differences, being shorter in BD males, compared to control males, and longer in healthy males, compared to control females.

To evaluate the use of biofeedback intervention in the levels of depression. The main hypothesis tested if the use of biofeedback improves depression levels compared to the control group.

A randomised clinical trial. The final sample was composed of 36 participants (18 in the experimental group, receiving 6 training, once a week, with biofeedback; and 18 in the control group, who received conventional treatment in the service).Outcome measures were assessed in two stages: pre-test and post-test. The research used the following instruments: demographic survey data, Mini International Neuropsychiatric Interview 5.0.0 and Beck Depression Inventory (BDI). The factors and variables were presented in terms of descriptive and inferential statistics. Fisher’s exact test (p < 0.05) was used to verify the existence of an association between the counting variables. The multinomial logistic regression model was adopted, and the Logit link function was used, as the software RStudio version 3.6.2.

The factors that remained in the final model were group, sex, partner, atypical antidepressant, benzodiazepines, mood stabiliser, antiepileptic and antihistamine, according to the levels of depression based on the BDI. The group that did not receive biofeedback intervention had 16 times more chances of increasing the depression levels compared to participants in the experimental group.

The use of biofeedback reduces depression, thus, representing a complementary alternative for the treatment of moderate and severe depression, and dysthymia.

Cross-sectional data show that post-traumatic stress disorder (PTSD) patients often have increased levels of circulating inflammatory markers. There is, however, still a paucity of longitudinal studies with long follow-up times on levels of cytokines in such patients. The current study assesses patients with and without PTSD diagnosis 1 year after discharge from inpatient treatment.

Patients in treatment for serious non-psychotic mental disorders were recruited at the beginning of their treatment stay at a psychiatric centre in Norway. Ninety patients submitted serum samples and filled out the Hopkins Symptom Checklist-90 Revised Global Severity Index (HSCL-90R GSI) questionnaire during their mainstay and at a follow-up stay 1 year after discharge. Of these patients, 33 were diagnosed with PTSD, 48 with anxiety, depression, or eating disorder, while 9 patients had missing data. The patients were diagnosed using the Mini-International Neuropsychiatric Interview (MINI).

At the follow-up stay (T3), PTSD patients had higher levels of GSI scores than non-PTSD patients (p = 0.048). These levels were unchanged from the year before (T2) in both groups. The levels of circulating cytokines/chemokine did not differ between the PTSD and non-PTSD patients at T3. At T2, however, the PTSD and non-PTSD groups exhibited different levels of interleukin 1β (IL-1β) (p = 0.053), IL-1RA (p = 0.042), and TNF-α (p = 0.037), with the PTSD patients having the higher levels.

Despite exhibiting different mental distress scores, the PTSD and non-PTSD patients did not differ regarding levels of circulating inflammatory markers at 1-year follow-up.

A few former studies suggested that there are partial overlaps in abnormal brain structure and cognitive function between hypochondriasis (HS) and schizophrenia (SZ). But their differences in brain activity and cognitive function were unclear.

Twenty-one HS patients, 23 SZ patients, and 24 healthy controls (HC) underwent resting-state functional magnetic resonance imaging (rs-fMRI) with the regional homogeneity analysis (ReHo), subsequently exploring the relationship between ReHo value and cognitive functions. The support vector machines (SVM) were used on effectiveness evaluation of ReHo for differentiating HS from SZ.

Compared with HC, HS showed significantly increased ReHo values in right middle temporal gyrus (MTG), left inferior parietal lobe (IPL), and right fusiform gyrus (FG), while SZ showed increased ReHo in left insula, decreased ReHo values in right paracentral lobule. Additionally, HS showed significantly higher ReHo values in FG, MTG, and left paracentral lobule, but lower in insula than SZ. The higher ReHo values in insula were associated with worse performance in MATRICS consensus cognitive battery (MCCB) in HS group. SVM analysis showed a combination of the ReHo values in insula and FG was able to satisfactorily distinguish the HS and SZ patients.

Our results suggested that the altered default mode network (DMN), of which abnormal spontaneous neural activity occurs in multiple brain regions, might play a key role in the pathogenesis of HS, and the resting-state alterations of insula are closely related to cognitive dysfunction in HS. Furthermore, the combination of the ReHo in FG and insula was a relatively ideal indicator to distinguish HS from SZ.

G protein-coupled receptor 55 (GPR55) is an orphan G protein-coupled receptor with various physiological functions. Recent evidence suggests that this receptor may be involved in the control of motor functions. Therefore, in the present study, we evaluated the effects of intra-striatal administration of GPR55 selective ligands in a rat model of Parkinson’s disease.

Experimental Parkinson was induced by unilateral intra-striatal administration of 6-hydroxydopamine (6-OHDA, 10 µg/rat). L-α-lysophosphatidylinositol (LPI, 1 and 5 µg/rat), an endogenous GPR55 agonist, and ML193 (1 and 5 µg/rat), a selective GPR55 antagonist, were injected into the striatum of 6-OHDA-lesioned rats. Motor performance and balance skills were evaluated using the accelerating rotating rod and the ledged beam tests. The sensorimotor function of the forelimbs and locomotor activity were assessed by the adhesive removal and open field tests, respectively.

6-OHDA-lesioned rats had impaired behaviours in all tests. Intra-striatal administration of LPI in 6-OHDA-lesioned rats increased time on the rotarod, decreased latency to remove the label, with no significant effect on slip steps, and locomotor activity. Intra-striatal administration of ML193 also increased time on the rotarod, decreased latency to remove the label and slip steps in 6-OHDA-lesioned rats mostly at the dose of 1 µg/rat.

This study suggests that the striatal GPR55 is involved in the control of motor functions. However, considering the similar effects of GPR55 agonist and antagonist, it may be concluded that this receptor has a modulatory role in the control of motor deficits in an experimental model of Parkinson.

Dietary lipids (omega-3 polyunsaturated fatty acids (n-3) PUFAs) and saturated fatty acids (SFA) seem to play an important role in brain health. (n-3) PUFAs have been shown to improve cerebral perfusion and to promote synaptogenesis. In this study, we investigated the relationship between dietary fat composition, cognitive performance and brain morphology in cognitively healthy individuals.

A total of 101 cognitively healthy participants (age: 42.3 ± 21.3 years, 62 females) were included in this study. Verbal memory was assessed using the California Verbal Learning Test (CVLT). Intake of (n-3) PUFA and SFA was calculated from food-frequency questionnaire-derived data (EPIC-FFQ). Magnetic resonance imaging (MRI) data were obtained (Siemens Trio 3T scanner) and grey matter volumes (GMV) were assessed by voxel-based morphometry (VBM/SPM8). We examined the association of SFA/(n-3) PUFA ratio and memory performance as well as GMV using regression models adjusted for age, sex, education, body mass index, apolipoprotein E (APOE) status and alcohol consumption. For VBM data, a multiple regression analysis was performed using the same covariates as mentioned before with intracranial volume as an additional covariate.

A high SFA/(n-3) PUFA ratio was significantly (p < 0.05) correlated with poorer verbal memory performance and with lower GMV in areas of the left prefrontal cortex that support memory processes.

These findings suggest that a diet rich in PUFAs is likely to exert favourable effects on brain morphology in brain areas important for memory and executive functions. This could constitute a possible mechanism for maintaining cognitive health in older age.

We have often observed dementia symptoms or severe neurocognitive decline in the long-term course of schizophrenia. While there are epidemiological reports that patients with schizophrenia are at an increased risk of developing dementia, there are also neuropathological reports that the prevalence of Alzheimer’s disease (AD) in schizophrenia is similar to that in normal controls. It is difficult to distinguish, based solely on the clinical symptoms, whether the remarkable dementia symptoms and cognitive decline seen in elderly schizophrenia are due to the course of the disease itself or a concomitant neurocognitive disease. Neuropathological observation is needed for discrimination.

We conducted a neuropathological search on three cases of schizophrenia that developed cognitive decline or dementia symptoms after a long illness course of schizophrenia. The clinical symptoms of total disease course were confirmed retrospectively in the medical record. We have evaluated neuropathological diagnosis based on not only Hematoxylin–Eosin and Klüver–Barrera staining specimens but also immunohistochemical stained specimens including tau, β-amyloid, pTDP-43 and α-synuclein protein throughout clinicopathological conference with multiple neuropathologists and psychiatrists.

The three cases showed no significant pathological findings or preclinical degenerative findings, and poor findings consistent with symptoms of dementia were noted.

Although the biological background of dementia symptoms in elderly schizophrenic patients is still unclear, regarding the brain capacity/cognitive reserve ability, preclinical neurodegeneration changes in combination with certain brain vulnerabilities due to schizophrenia itself are thought to induce dementia syndrome and severe cognitive decline.