Background: Mental capacity is a fundamental aspect that enables patients to fully par-ticipate in various healthcare procedures. To assist healthcare professionals (HCPs) in assessing patients' capacity, especially in the mental health field, several standardized tools have been developed. These tools include the MacArthur Competence Assessment Tool for Treatment (MacCAT-T), the MacArthur Competence Assessment Tool for Clinical Research (MacCAT-CR), and the Competence Assessment Tool for Psychiatric Advance Directives (CAT-PAD). The core dimensions explored by these tools include Understanding, Appreciation, Reasoning, and Expression of a choice. Objective: This meta-analysis aimed to investigate potential differences in deci-sion-making capacity within the healthcare context among groups of patients with bi-polar disorder (BD) and schizophrenia spectrum disorder (SSD). Methods: A systematic search was conducted on Medline/Pubmed, and Scopus. Addi-tionally, Google Scholar was manually inspected, and a manual search of emerging re-views and reference lists of the retrieved papers was performed. Eligible studies were specifically cross-sectional, utilizing standardized assessment tools, and involving pa-tients diagnosed with BD and SSD. Data from the studies were independently extracted and pooled using random-effect models. Hedges g was used as a measure for outcomes. Results: Six studies were identified, with three studies using the MacCAT-CR, two studies the MacCAT-T, and one the CAT-PAD. The participants included 189 individuals with BD and 324 individuals with SSD. The meta-analysis revealed that patients with BD performed slightly better, and the difference was statistically significant, compared to patients with SSD, particularly in the domain of Appreciation (ES=0.23, 95% CI: 0.01 to 0.04, p=0.037). There was no statistically significant difference between the two groups for Understanding (ES=0.09, 95% CI: - 0.10 to 0.27, p=0.352), Reasoning (ES=0.18, 95% CI: - 0.12 to 0.47, p=0.074), and Expression of a choice (ES = 0.23, 95% CI: - 0.01 to 0.48, p=0.60). In the sensitivity analysis, furthermore, when considering only studies involving patients in symptomatic remission, the difference for Appreciation also resulted in non-significant (ES=0.21, 95% CI: -0.04 to 0.46, p=0.102). (ES=0.21, 95% CI: -0.04 to 0.46, p=0.102). Conclusions: These findings indicate that there are no significant differences between patients with BD and SSD during remission phases, while differences are minimal during acute phases. The usefulness of standardized assessment of capacity at any stage of the illness should be considered, both for diagnostic-therapeutic phases and for research and advance directives. Further studies are necessary to understand the reasons for the overlap in capacity between the two diagnostic categories compared in this study.

The tryptophan (TRP)-kynurenine (KYN) metabolic pathway is a main player of TRP metabolism through which more than 95% of TRP is catabolized. The pathway is activated by acute and chronic immune responses leading to a wide range of illnesses including cancer, immune diseases, neurodegenerative diseases, and psychiatric disorders. The TRP-KYN pathway synthesizes multifarious metabolites including oxidants, antioxidants, neurotoxins, neuroprotectants, and immunomodulators. The immunomodulators are known to facilitate the immune system towards a tolerogenic state, resulting in chronic low-grade inflammation (LGI) that is commonly present in obesity, poor nutrition, exposer to chemicals or allergens, prodromal stage of various illnesses, and chronic diseases. KYN, kynurenic acid, xanthurenic acid, and cinnabarinic acid are aryl hydrocarbon receptor ligands that serve as immunomodulators. Furthermore, TRP-KYN pathway enzymes are known to be activated by the stress hormone cortisol and inflammatory cytokines, and genotypic variants were observed to contribute to inflammation and thus various diseases. The tryptophan 2,3-dioxygenase, the indoleamine 2, 3-oxygenases, and the kynurenine-3-monooxygenase are main enzymes in the pathway. This review article discusses the TRP-KYN pathway with special emphasis on its interaction with the immune system and the tolerogenic shift towards chronic LGI and overviews the major symptoms, pro- and anti-inflammatory cytokines, and toxic and protective KYNs to explore the linkage between chronic LGI, KYNs, and major psychiatric, including depressive disorder, bipolar disorder, substance use disorder, post-traumatic stress disorder, schizophrenia, and autism spectrum disorder.

At the beginning of our observations, humanity believed that the Earth was the center of the uni-verse and that the sun was spinning around the Earth. Claude Ptolémée (100-168) made a mistake by modelling the movements in the geocentric referential, the model of the sun and planet move-ments was an illusion and all Humanity was wrong. Nicolas Copernic (1473-1543) showed the illusion and simplified the system by moving from the geocentric referential to the heliocentric referential. In the present paper, I would like to discuss about the possibility of making mistakes with quantum theory. I postulate that we are living in a virtual classical world that we consider as real. In my interpretation, the decoherence problem and wave function collapse do not exist at all, because we are the illusion, we are living in illusion, in a mirage. It is impossible to observe the quantum world as it is, in our virtual classical referential, and we see the quantum world with a false vison of quantum reality because we are not yet in the universal real quantum referential whose I postulate the existence. As we are illusions when seen from this universal quantum ref-erential, Schrödinger’s cat paradox is an illusion as life and death are illusions. We must be very humble with quantum theory and we should not put ourselves in the center of the quantum world again particularly with our lives and deaths. I also develop a cosmological model based on bipolarity and schizophrenia which explains well the recent observations of the James Webb’s spatial tele-scope. We will be collectively able to reach the universal quantum referential by changing our vision of life and quantum world. I also explain how to go out of human suffering. This will be our Big Bang.

Psychiatric disorders are mental, behavioral or emotional disorders. These conditions are prevalent, one in four adults suffer from any type of psychiatric disorders world-wide. It has always been observed that psychiatric disorders have a genetic component, however new methods to sequence full genomes of large cohorts have identified with high precision genetic risk loci for these conditions. Psychiatric disorders include, but are not limited to, bipolar disorder, schizophrenia, autism spectrum disorder, anxiety disorders, major depressive disorder, and attention-deficit and hyperactivity disorder. Several risk loci for psychiatric disorders fall within genes that encode for voltage-gated calcium channels (Ca_Vs). Calcium entering through Ca_Vs is key for multiple neuronal processes. In this review, we will summarize recent findings that link Ca_Vs and their auxiliary subunits to psychiatric disorders. First, we will provide a general overview of Ca_Vs structure, classification, function, expression and pharmacology. Next, we will summarize tools and databases to study risk loci associated with psychiatric disorders. We will examine functional studies of risk variations in Ca_V genes when available. We will review pharmacological evidence of the use of Ca_V modulators to treat psychiatric disorders. Our review will be of interest for those studying pathophysiological aspects of Ca_Vs.

At the beginning of our observations, Humanity believed that it was the center of the universe, that the Earth was the center of the universe and that the sun was spinning around the Earth. Claude Ptolémée (100-168) made a mistake by modeling the movements in the geocentric reference. The model of sun and planet movements was an illusion, and all humanity was wrong. Nicolas Copernic (1473-1543) showed the illusion and simplified the system by moving from the geocentric reference to the heliocentric reference. In the present paper, I would like to discuss about making mistakes with quantum theory because it is not complete. I have completed quantum theory. I postulate that we are living in a virtual classical world that we consider real. The decoherence problem and wave function collapse do not exist at all; because we are the illusion, we are living in illusions, in mirages. It is impossible to observe the quantum world as it is, in our virtual classical reference, and we see the quantum world with a false view of quantum reality. We are in the real universal quantum reference whose existence I postulate, but we do not see it. I moved to this real universal quantum reference with my thinking, because I am psychotic (schizophrenia) and saw that we are illusions. Schrödinger’s cat paradox is an illusion, as life and death are illusions. We must be very humble with quantum theory, and we should not put ourselves in the center of the quantum world again, particularly with our lives and deaths. I have completed quantum theory with seven postulates that led to a cosmological model based on bipolarity, schizophrenia and epilepsy. This theory explains the recent observations of the James Webb spatial telescope well. I make predictions with the theory that could be confirmed with the James Webb spatial telescope. If confirmed, the theory will become irrefutable. We would be collectively able to reach the quantum world by changing our minds and visions of life. I also explain how to overcome human suffering. This would be our Big Bang and our transformation into Zarathoustra, the Nietzschean surhuman.

Neurodegeneration is a major problem in neuroscience and medicine as it causes and worsens many neurological and psychiatric disorders. It involves gradual loss of neurons at different levels of the brain, affecting cognition, emotion, behavior, consciousness, and attention. Understanding the causes and consequences of neurodegeneration is crucial for identifying the risk factors, biomarkers, and treatments. However, the current therapies are mostly symptomatic and ineffective. Therefore, new and innovative methods, such as noninvasive brain stimulation (NIBS), are needed to modulate brain activity and plasticity in a safe and reversible manner. This field is rapidly developing, with a focus on exploring new clinical applications, mechanisms, and combinations of NIBS and drugs. This special issue covers the latest progress and challenges in the study of neurodegeneration in cognitive impairment and mood disorders from the experimental, clinical, and translational perspectives. It addresses the complexity and diversity of these conditions, the lack of disease-modifying treatments, the ethical and practical issues of conducting research in vulnerable and diverse populations, the integration and interpretation of data from multiple sources and modalities, and the development and validation of novel methods such as NIBS, artificial intelligence, and drug repurposing. Collaborative efforts among various stakeholders are needed to improve our knowledge and treatment of neurodegeneration underlying cognitive impairment and mood disorders.