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There is still no basic overview about the effect of various types of comorbidity in executive functions due to two main reasons: (1) the type and number of comorbidities in ADHD is significantly varied, (2) EFs are very diverse and have different neuropsychological properties. Our objective was to determine the effect of comorbid disorders (number and type) on the performance in a wide range (seven) of executive functions in a sample of children with ADHD. Fifty-five male children aged seven to nine years with ADHD were divided into six groups: G1 = ADHD only (ADHD-O), G1 = Oppositional defiant disorder (ODD), G3 = (anxiety/depressive disorder (ADD), G4 = ODD + ADD, G5 = ODD + learning disorder (LD), G6 = ODD + LD + conduct disorder (CD). The six groups exhibited different number of deficits in EFs; G1 showed only 1 deficit in contrast, G6 presented 11. Statistical analysis (ANOVA and logistic regression) identified three most affected EFs: Working memory, generation/classification of semantic categories, and inhibitory control. Alterations in EFs increased mainly in relation to the increase of the specific number and type of comorbidity. To date, no studies have addressed comorbidity from this perspective. A wide range approach of EF confirms the need to further study comorbidity in ADHD from a wide range/variety perspective and determine all possible combinations (number/type) to clarify its contribution to the complex neuropsychology functioning in ADHD.

Coronaviruses are neurotropic viruses capable of entering the brain through various mechanisms and generating an important inflammatory response that is capable of triggering neuropsychiatric manifestations. Several reports describe the appearance of different conditions, such as sleep problems, anxiety and depression disorders, acute psychotic disorders, encephalitis, and delirium, among others, associated with COVID-19 infection. We performed a literature review in PubMed, Springer, Nature, MDPI, and other scientific journals on the relationship between COVID-19 infection with the development and aggravation of neuropsychiatric manifestations explained by molecular changes secondary to SARS-CoV-2 where it was found that there is a relationship between the virus and the development of these manifestations. Prospective neuropsychiatric follow-up of people exposed to SARS-CoV-2 at different points in their lives, as well as their neuroimmunological status, is necessary to fully understand the long-term impact of COVID-19 on mental health. It is required to identify the risk of developing neuropsychiatric problems due to COVID-19 infection to provide better medical care from a multidisciplinary team and improve the prognosis of these patients as well as the treatment of long-term sequelae.

Research reported that sucralose induces metabolic derangements via gut microbiota modulation. However, rebaudioside A (reb A) exposure on gut microbiota has barely been evaluated. The aim of this study was to examine the gut microbiota response to sucralose or reb A in rats under two dietary conditions. Male Wistar rats (150–200 g) on normal diet (ND) or high-fat diet (HFD) were randomized to receive sucralose (SCL), reb A (REB), glucose (GLU, control), or sucrose (SUC). After eight weeks, fecal samples were analyzed by 16S ribosomal RNA gene sequencing. The diversity and the structure of the gut microbiota were not modified by NNS. In ND rats, SCL decreased phylum Firmicutes and increased Bacteroidetes and its genus Bacteroidia. At class level, in HFD rats, REB reduced Bacilli proportions. The genus Romboutsia was reduced with SCL and REB along ND. Lactobacillus increased with SCL and reduced with REB in HFD. After comparative analyses between the two types of diets, we observed that only HFD in combination with SCL increased Bacilli and diminished Bacteroidiaabundances relative to ND. Exposure to NNS, at equivalent doses to the ADI, slightly induce modifications on gut microbiota in ND and HFD feeding rats, and the effects were more pronounced with sucralose ingestion combined with the HFD regimen. Further studies are needed to examine the potential mechanisms involved.

BackgroundThe aim of this study is to identify differentially methylated regions (DMRs) in the genomes of a sample of cognitively healthy individuals and a sample of individuals with LOAD, all of them nonagenarians from Costa Rica.MethodsIn this study, we compared whole blood DNA methylation profiles of 32 individuals: 21 cognitively healthy and 11 with LOAD, using the Infinium MethylationEPIC BeadChip. First, we calculated the epigenetic age of the participants based on Horvath’s epigenetic clock. DMRcate and Bumphunter were used to identify DMRs. After in silico and knowledge-based filtering of the DMRs, we performed a methylation quantitative loci (mQTL) analysis (rs708727 and rs960603).ResultsOn average, the epigenetic age was 73 years in both groups, which represents a difference of over 20 years between epigenetic and chronological age in both affected and unaffected individuals. Methylation analysis revealed 11 DMRs between groups, which contain six genes and two pseudogenes. These genes are involved in cell cycle regulation, embryogenesis, synthesis of ceramides, and migration of interneurons to the cerebral cortex. One of the six genes is PM20D1, for which altered expression has been reported in LOAD. After genotyping previously reported mQTL SNPs for the gene, we found that average methylation in the PM20D1 DMR differs between genotypes for rs708727, but not for rs960603.ConclusionsThis work supports the possible role of PM20D1 in protection against AD, by showing differential methylation in blood of affected and unaffected nonagenarians. Our results also support the influence of genetic factors on PM20D1 methylation levels.

Suicide attempts are an emerging health problem around the world. Increased levels of IL-6 have been associated with suicidal behavior. Therefore, the aims of this study were to evaluate the serum levels of IL-6 in individuals with suicide attempts and a comparison group and to associate the IL-6 levels with the lethality of the suicide attempt. Additionally, we associated the rs2228145 polymorphism of the IL6R gene with suicide attempts or with the IL-6 serum levels. Suicide attempts and their lethality were evaluated using the Columbia Suicide Severity Rating Scale. The serum concentrations of IL-6 were measured by the ELISA technique in individuals with suicide attempts and then compared to a control group. The rs2228145 polymorphism of the IL6R gene was analyzed by real-time polymerase chain reaction. We found elevated serum levels of IL-6 in the suicide attempt group when compared to the control group (F = 10.37, p = 0.002). However, we found no differences of the IL-6 levels between high and low lethality. The IL6R gene polymorphism rs2479409 was not associated with suicide attempts. Our data suggest that IL-6 serum is increased in individuals with suicide attempts.

Introduction: Obsessive-compulsive disorder (OCD), characterized by repetitive anxiety-inducing intrusive thoughts and compulsive behaviors, is associated with higher suicide ideation and suicide attempts than the general population. This study investigates the prevalence and the correlates of current suicide risk in adult outpatients in an international multisite cross-sectional sample of OCD outpatients. Methods: Data were derived from the International College of Obsessive-Compulsive Spectrum Disorders (ICOCS) network's cross-sectional data set (N = 409). Current suicide risk (assessed by Item C of the MINI) and diagnoses of psychiatric disorders were based on DSM-IV. Chi-squared test for categorical variables and t-test for continuous variables were used to make statistical inferences about main features associated with current suicide risk. P < .05 was considered as statistically significant. Results: The prevalence of current suicidal risk was 15.9%, with equal likelihood in sociodemographic variables, including age and gender. Increased rates of major depression and generalized anxiety disorder were associated to higher current suicide risk. Current suicide risk was also associated with higher severity of OCD, depressive comorbidity, and higher levels of disability. There were no significant differences in treatment correlates—including type of treatment and psychiatric hospitalizations—between the groups of individuals with and without current suicide risk. Conclusion: Our findings suggest that current suicide risk is common in patients with OCD and associated with various forms of pathology. Our work also provides further empirical data to support what is already known clinically: a worse clinical picture characterized by a high severity of OCD, high distress related to obsessions and compulsions, and the presence of comorbidities such as major depression and generalized anxiety disorder should be considered as relevant risk factors for suicide risk.

Several studies have evaluated the possible association between polymorphisms or variants in Corticotropin-releasing hormone 1 receptor gene (CRHR1) with depression; however, results remain contradictory and heterogeneous. To our knowledge, we conducted the first comprehensive systematic review and meta-analysis evaluating the association of the CRHR1 gene and the risk of depression. A search online was conducted in databases for any CRHR1 genetic association studies in depression. Data were extracted for evaluation of pooled estimates using meta-analytic techniques. Statistical analyses were performed using the Comprehensive Meta-analysis, v2.0 software. A total of 1403 cases and 2353 mentally healthy controls were included in this study. We found a significant association of rs242941, rs1876828 and rs242939 variants of the CRHR1 gene with depression. No association of CRHR1 rs110402 and depression was observed. Our meta-analysis shows that some variants of the CRHR1 gene (rs242941, rs1876828 and rs242939) might confer susceptibility to depression. Further studies with larger sample sizes need to be conducted.

Background Suicide represents a major health concern, especially in developing countries. While many demographic risk factors have been proposed, the underlying molecular pathology of suicide remains poorly understood. A body of evidence suggests that aberrant DNA methylation and expression is involved. In this study, we examined DNA methylation profiles and concordant gene expression changes in the prefrontal cortex of Mexicans who died by suicide. Methods In collaboration with the coroner’s office in Mexico City, brain samples of males who died by suicide (n = 35) and age-matched sudden death controls (n = 13) were collected. DNA and RNA were extracted from prefrontal cortex tissue and analyzed with the Infinium Methylation480k and the HumanHT-12 v4 Expression Beadchips, respectively. Results We report evidence of altered DNA methylation profiles at 4430 genomic regions together with 622 genes characterized by differential expression in cases vs controls. Seventy genes were found to have concordant methylation and expression changes. Metacore-enriched analysis identified 10 genes with biological relevance to psychiatric phenotypes and suicide (ADCY9, CRH, NFATC4, ABCC8, HMGA1, KAT2A, EPHA2, TRRAP, CD22, and CBLN1) and highlighted the association that ADCY9 has with various pathways, including signal transduction regulated by the cAMP-responsive element modulator, neurophysiological process regulated by the corticotrophin-releasing hormone, and synaptic plasticity. We therefore went on to validate the observed hypomethylation of ADCY9 in cases vs control through targeted bisulfite sequencing. Conclusion Our study represents the first, to our knowledge, analysis of DNA methylation and gene expression associated with suicide in a Mexican population using postmortem brain, providing novel insights for convergent molecular alterations associated with suicide.

Suicides and homicides are public health problems around the world. The rates of suicide and homicide have increased in the past years. The objectives of this study are to estimate the rates of suicide and homicide in Mexico City, and to determine the rates of suicide and homicide by sex in the different municipalities of Mexico City during 2019. Data analyzed were obtained from files of governmental organizations in Mexico City. From the general victims-in-research-folders, we choose “victims of crime” or “loss of life by suicide” that happened in 2019. Sex and municipality of residence were obtained. The rate of suicide was of 5.65 cases per 100,000 habitants. Stratified by gender and by municipalities, the highest rates observed were 6.8 suicides per 100,000 males and 29.6 suicides per 100,000 females. The sex ratio was 4.2:1 (males: females). Regarding homicides, the rates were 16.68 homicides per 100,000 females and 67.41 homicides per 100,000 males. The Venustiano Carranza Municipality showed the highest homicide rate in men with 131.72 homicides per 100,000 males. The homicide sex ratio was 7.8:1. The findings of the present study highlight that death by suicide is more common in men with 7.8 more times than in women. The municipalities with higher deaths by suicide have lower rates of homicides and the municipalities with higher deaths by suicide showed lower rates of suicide in men.

Resumen Antecedentes La aceleracion del reloj epigenetico se ha asociado con una reduccion en la esperanza de vida. Los individuos con diagnostico de algun trastorno psiquiatrico presentan una reduccion en la esperanza de vida, y algunos estudios la han correlacionado con un envejecimiento acelerado. Objetivo El presente estudio tiene el objetivo de explorar si la presencia de algun trastorno psiquiatrico podria acelerar el reloj epigenetico en gemelos monocigoticos. Metodos Se incluyeron un total de 15 pares de gemelos monocigoticos. La edad epigenetica en celulas de sangre periferica fue estimada mediante algoritmos publicados previamente, utilizando el microarreglo 450 K Beadchip. Resultados Encontramos que en los gemelos con diagnostico de algun trastorno psiquiatrico podria aumentar el reloj epigenetico en comparacion con su gemelo sin trastorno psiquiatrico. Discusion y conclusion La presencia de algun trastorno psiquiatrico podria acelerar el reloj epigenetico en gemelos homocigoticos, pero se requieren estudios con muestras de mayor tamano para aclarar esta relacion.

Objective. To explore whether maternal sensitivity is associated with Autism Spectrum Disorder (ASD) severity in children with and without ASD. Design. The samples consisted of 25 Mexican dyads of children with ASD (aged 3.1-6.9 years) and their mothers (aged 20-47 years) and 24 Mexican dyads of children without ASD (aged 3.4-6.7 years) and their mothers (aged 24-45 years). Maternal sensitivity and ASD severity symptoms were scored from 2-h videos of mother-child daily interactions. Results. A between-group comparison showed a trend toward less severe ASD in children with highly sensitive mothers, specifically in the Nonverbal Communication subdomain. Conclusions. Greater maternal sensitivity is associated with improved social ability in children with ASD.

The COVID-19 pandemic has had an impact on mental health in the general population, but no systematic synthesis of evidence of this effect has been undertaken for the Mexican population. Relevant studies were identified through the systematic search in five databases until December, 2021. The selection of studies and the evaluation of their methodological quality were performed in pairs. The Newcastle-Ottawa Scale (NOS) was used for study quality appraisal. The protocol of this systematic review was registered with PROSPERO (protocol ID: CRD42021278868). This review included 15 studies, which ranged from 252 to 9361 participants, with a total of 26,799 participants. The findings show that COVID-19 has an impact on the Mexican population’s mental health and is particularly associated with anxiety, depression, stress and distress. Females and younger age are risk factors for development mental health symptoms. Mitigating the negative effects of COVID-19 on mental health should be a public health priority in Mexico.

Objective: Individuals with schizophrenia and substance use disorders have a poor prognosis and increased psychiatric symptoms. The present study aimed to explore the association of 106 genes in individuals with schizophrenia and comorbid substance use through a next-generation sequencing (NGS) analysis and different in silico algorithms. Methods: We included 105 individuals diagnosed with schizophrenia and a family history of schizophrenia, of whom 49 (46.67%) presented comorbid substance use. Using NGS, we sequenced 106 genes previously associated with schizophrenia. Logistic regression models were used to assess differences in allele frequencies, and a generalized gene-set analysis was performed at the gene level. Functional annotations were performed using different algorithms and databases. Results: We identified a total of 3,109 variants, of which 25 were associated with schizophrenia and comorbid substance use and were located in regulatory and coding regions. We found low-frequency variants in COMT p.Ala72Ser, independently of p.Val158Met, that were associated with substance use. The endocannabinoid functional variant FAAH p.Pro129Thr was also associated with substance use. Conclusions: Genetic variants of genes related to dopaminergic and cannabinoid neurotransmitter systems were associated with comorbid substance use in schizophrenia. Nevertheless, more studies with larger sample sizes are needed to confirm our findings.

The development and use of advanced and innovative neuroscience, neurotechnology and some forms of artificial intelligence have exposed potential threats to the human condition, including human rights. As a result, reconceptualizing or creating human rights (i.e. neurorights) has been proposed to address specific brain and mind issues like free will, personal identity and cognitive liberty. However, perceptions, interpretations and meanings of these issues-and of neurorights-may vary between countries, contexts and cultures, all relevant for an international-consensus definition and implementation of neurorights. Thus, we encourage reflecting on the proactive inclusion of transnational, cross-cultural and contextual considerations and concerns to contribute to the global discourse. This inclusion does not mean endorsing ethical relativism but rather a call to foster a universal understanding of key concepts and concerns. Including contextual and cultural perspectives may truly anticipate global concerns which could be addressed while developing and implementing neurorights. Consequently, any ethical and/or legal regulatory framework(s) for the translational and transnational use of advanced neuroscience, neurotechnology and some forms of artificial intelligence intended to protect and safeguard human dignity should be contextually and culturally mindful, responsible, respectful and inclusive of not only human rights and fundamental freedoms but also of neurocognitive cultural diversity.

Introduction. It has been hypothesized that pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections (PANDAS) etiology results from an abnormal immune response to streptococcal infection. There is evidence that the serotonergic system is involved in both obsessive-compulsive disorder (OCD) physiopathology and immunological processes. In the 5’ promoter region of 5-HTT, gene encoding for the serotonin transporter we can find the 5-HTTLPR polymorphism that has been associated with OCD. Being PANDAS a disorder with OCD symptoms and likely immune abnormalities, 5-HTT polymorphisms may be particularly relevant for this disorder. Objective. This study aimed to test the association between the 5-HT genotypes and the presence of serum antibodies in patients with PANDAS. Method. We compared the genotype frequencies and serum anti-streptococcal, anti-neural, and anti-enolase antibodies titers between 56 patients with PANDAS and 20 healthy controls from Mexico and Cuba. Results. Antibody titers were higher (anti-enolase, anti-streptococcal) in PANDAS patients compared to healthy controls. No differences in anti-neural antibody levels between both groups were detected. The anti-enolase and anti-neural antibody titer increased according to the polymorphism of the PANDAS patients as follows: LL >SL >SS. Discussion and conclusion. This is the first study evaluating the association between the 5-HTTLPR genotypes and antibody titers in PANDAS patients. Associations between polymorphisms in serotonergic genes and immune response could provide valuable information about the interaction between both systems. Our results suggest an association between the S allele and elevated antibody levels in PANDAS patients.

espanolIntroduccion. Se han identificado algunos factores de riesgo para el trastorno del espectro autista (TEA) como es el caso de la edad parental avanzada. La edad parental avanzada es un factor de riesgo que ha sido muy explorado en poblaciones escandinavas; sin embargo, no existen reportes en ninos de ascendencia mexicana. Objetivo. El presente trabajo tiene el objetivo de analizar si la edad parental avanzada es un factor de riesgo para TEA en una muestra de ninos mexicanos. Metodo. Un total de 1 068 ninos de la Ciudad de Mexico se incluyeron en un estudio de casos-controles, de los cuales 162 contaban con diagnostico de TEA. Regresiones logisticas multivariable, ajustadas por confusores, se realizaron para explorar el efecto de la edad parental avanzada en el riesgo para TEA. Resultados. La edad paterna avanzada en ninos mexicanos aumento el riesgo para TEA; tambien, una diferencia de edad de 10 anos entre los padres presenta un mayor riesgo. Discusion y conclusion. El efecto de la edad paterna avanzada en los ninos mexicanos fue mucho mas bajo que aquella reportada para otras poblaciones. La edad paterna avanzada y la diferencia entre la edad parental puede ser un factor de riesgo para TEA en poblacion mexicana. Sin embargo, se requieren analisis en poblaciones con mayor tamano de muestra EnglishIntroduction. Risk factors for autism spectrum disorders (ASD) have been identified, as is the case of advanced parental age. Advanced parental age as an ASD risk factor has been studied in Scandinavian populations; there are no reports for Mexican children. Objective. The present work aim is to analyze if advanced parental age is a risk factor for ASD in a Mexican children sample. Method. Mexican children (N = 1 068) participated in a case-control study, 162 had an ASD diagnosis. Multivariate logistic regression adjusted by cofounders was performed to explore the effect of paternal age on ASD risk. Results. Advanced paternal age in Mexican children increases the risk for ASD, and also, a difference of 10 years between parental ages have a higher risk. Discussion and conclusion. The effect of advanced paternal age in Mexican children was lower than those reported previously for other populations. Advanced paternal age and difference between parental ages could be a risk factor for ASD in Mexican population. Nevertheless, the analysis of larger sample sizes is required.

Suicidal behavior is result of the interaction of several contributors, including genetic and environmental factors. The integration of approaches considering the polygenic component of suicidal behavior, such as polygenic risk scores (PRS) and DNA methylation is promising for improving our understanding of the complex interplay between genetic and environmental factors in this behavior. The aim of this study was the evaluation of DNA methylation differences between individuals with high and low genetic burden for suicidality. The present study was divided into two phases. In the first phase, genotyping with the Psycharray chip was performed in a discovery sample of 568 Mexican individuals, of which 149 had suicidal behavior (64 individuals with suicidal ideation, 50 with suicide attempt and 35 with completed suicide). Then, a PRS analysis based on summary statistics from the Psychiatric Genomic Consortium was performed in the discovery sample. In a second phase, we evaluated DNA methylation differences between individuals with high and low genetic burden for suicidality in a sub-sample of the discovery sample (target sample) of 94 subjects. We identified 153 differentially methylated sites between individuals with low and high-PRS. Among genes mapped to differentially methylated sites, we found genes involved in neurodevelopment (CHD7, RFX4, KCNA1, PLCB1, PITX1, NUMBL) and ATP binding (KIF7, NUBP2, KIF6, ATP8B1, ATP11A, CLCN7, MYLK, MAP2K5). Our results suggest that genetic variants might increase the predisposition to epigenetic variations in genes involved in neurodevelopment. This study highlights the possible implication of polygenic burden in the alteration of epigenetic changes in suicidal behavior.

Background:The last twenty years have seen major advancements in unraveling the etiology and the identification of biological markers of Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococci (PANDAS). However, this body of evidence has not yet been translated into a clinical setting.Objective:We will review the most important studies to date on PANDAS, emphasizing those whose advances could improve the diagnosis of these disorders. We also suggest the need for updated diagnosis criteria integrating the recent findings from the hereby included studies.Methods:Consulting the PubMed database, a literature review of the last twenty-one years (between 1998 and 2019) was carried out using the terms “PANDAS” and “pediatric autoimmune neuropsychiatric disorders” in combination with “diagnosis” and “markers”. The search resulted in 175 hits from which we selected clinical cases, original investigations, and clinical reviews.Results:This review offers a compilation of the most important studies performed to date regarding the clinical presentation and potential biological markers of PANDAS. Moreover, we suggest the refinement of some aspects in the current diagnosis criteria, such as focusing on specific symptoms and the inclusion of neuroimaging and peripheral markers.Conclusion:The identification of specific biological markers in PANDAS is crucial for its diagnosis and opportune treatment. Future research will determine whether PANDAS require separated diagnostic and therapeutic measures or if it should be included in recently proposed categories such as Pediatric Acute Neuropsychiatric Syndrome (PANS) or Childhood Acute Neuropsychiatric Syndrome (CANS).

There is little recent information about the prevalence of symptomatology of mental health disorders in representative population samples in Mexico. To determine the prevalence of mental health symptoms in Mexico and its comorbidity with tobacco, alcohol, and drug use disorder (SUD), we used the 2016–17 National Survey of Drug, Alcohol, and Tobacco Use (Encuesta Nacional de Consumo de Drogas, Alcohol y Tabaco, ENCODAT 2016–2017). The data were collected from households using a cross-sectional, stratified, multistage design, with a confidence level of 90% and a response rate of 73.6%. The final sample included 56,877 completed interviews of individuals aged 12–65, with a subsample of 13,130 who answered the section on mental health. Symptoms of mania and hypomania (7.9%), depression (6.4%), and post-traumatic stress (5.7%) were the three main problems reported. Of this subsample, 56.7% reported using a legal or illegal drug without SUD, 5.4% reported SUD at one time on alcohol, 0.8% on tobacco, and 1.3% on medical or illegal drugs, 15.9% reported symptoms related to mental health, and 2.9% comorbidity. The prevalence found is consistent with those reported in previous studies, except for an increase in post-traumatic stress, which is consistent with the country’s increase in trauma.

Background. From the first reports of the linguist Noam Chomsky it has become clear that the development of language has an important genetic component. Several reports in families have shown the relationship between language disorders and genetic polymorphisms. The FOXP2 gene has been a fundamental piece for the understanding of language development. This gene codes for a transcription factor containing a forkhead domain of DNA binding and participates in the regulation of the expression of a large number of genes involved in the embryonic development of fundamental neuronal structures needed for the development of speech and language. Objective. To present an updated view of the relationship between FOXP2 and language alterations in psychiatric pathology. Method. Narrative review of information reported in databases on the recent advances supporting genetic participation in language disorders of psychiatric illness. Results. Update of content related to FOXP2 and its participation in language alterations in psychiatric diseases. Discussion and conclusion. Advances in the genetic study of language disorders in psychiatric pathology open up new avenues of investigation that allow us to explore how language emerged and how it evolved, as well as to carry out comparative studies on the structure and functioning of genes to approach the understanding of this complex characteristic that makes us human.

To evaluate the progression by means of nuclear magnetic resonance of the lesion in the schizophrenia model of lesion of the ventral hippocampal nucleus (LVNH).Magnetic resonance imaging (MRI) were performed in male Wistar rats, from 8 days postnatal to 139 days, in animals with LNHV and without lesion (sham). The MRI were carried out on a Variant 7 T equipment. The data were analyzed with the Amira software, for a voxel-based morphometric analysis.We observed the presence of hypersignals with a significant enhancement in the structures analyzed in the group with LVNH, and greater volume in the lateral ventricles, presenting a larger size of the lesion on day PD96 and significantly reducing on day PD139.We found a cell rearrangement during the progression of the lesion, which could be the effect of the activation of immune cells.Evaluar mediante resonancia magnética (RM) la progresión de la lesión en el modelo de esquizofrenia de lesión del núcleo del hipocampo ventral (LNHV).Se realizaron RM en ratas Wistar macho, desde los 8 días posnatales hasta los 139 días, en animales con LNHV y sin lesión (sham). Las RM se realizaron con un equipo Variant de 7 T. Los datos se analizaron con el software Amira para un análisis de morfometría basada en vóxels.Observamos hiperseñales con un realce significativo en las estructuras analizadas en el grupo con LNHV, y mayor volumen en los ventrículos laterales, presentando un mayor tamaño de la lesión el día PD96 y significativamente reducido en el día PD139.Encontramos un reacomodo celular durante la progresión de la lesión, lo cual podría ser efecto de la activación de las células inmunitarias.

Obsessive-compulsive disorder (OCD) is a heritable disorder, but no definitive, replicated OCD susceptibility loci have yet been identified by any genome-wide association study (GWAS). Here, we report results from a GWAS in the largest OCD case-control sample (N = 14,140 OCD cases and N = 562,117 controls) to date. We explored the genetic architecture of OCD, including its genetic relationships to other psychiatric and non-psychiatric phenotypes. In the GWAS analysis, we identified one SNP associated with OCD at a genome-wide significant level. Subsequent gene-based analyses identified additional two genes as potentially implicated in OCD pathogenesis. All SNPs combined explained 16% of the heritability of OCD. We show sub-stantial positive genetic correlations between OCD and a range of psychiatric disorders, including anxiety disorders, anorexia nervosa, and major depression. We thus for the first time provide evidence of a genome-wide locus implicated in OCD and strengthen previous literature suggesting a polygenic nature of this disorder.

Cannabis is the most frequently consumed drug around the world. Its use has been associated with increased suicide behaviors; nonetheless, the association of cannabis smoking and suicide behaviors in adolescents has not yet been established. The aim of this systematic review and meta-analysis was to evaluate the risk of suicide attempt, suicidal ideation or suicide planning in individuals of 11-21 years of age who smoke cannabis.We performed an online searched using PubMed, EBSCO and Science Direct databases, up to July 2021. We calculated odds ratio with 95% confidence intervals to evaluate the association between suicide attempt, suicidal ideation or suicide planning and cannabis smoking in individuals of 11-21 years of age.Twenty studies reported suicide attempts in 34,859 young individuals, suicidal ideation in 26, 937 individuals, and suicide planning in 9054 young individuals. We found an increased risk of suicide attempt in cannabis smokers than in non-cannabis users (OR: 2.33; 95% CI: 1.78-3.05; Z p value;0.0001; IThis meta-analysis shows that cannabis smoking increased the risk of suicide attempt, suicidal ideation and suicide planning in young individuals of 11-21 years of age. The high risk of suicide behaviors could vary depending on the population studied; therefore, more studies are necessary to corroborate the risk of presenting suicide behaviors in individuals of 11-21 years of age who smoke cannabis.

Suicides and suicidal behavior are major causes of mortality and morbidity in public health and are a global problem. Various authors have proposed changes in lipid metabolism (total cholesterol decrease) as a possible biological marker for suicidal behavior. The objective of this study was to review the studies that have demonstrated a relationship between serum cholesterol levels and suicidal behavior and to describe the possible pathophysiological mechanisms that associate changes in cholesterol concentration and suicidal behavior. Relevant literature related to serum cholesterol levels and suicidal behavior was identified through various database searches. The data from the existing literature present the findings that relate low cholesterol levels and possible pathophysiological mechanisms (neuroinflammation, serotonergic neurotransmission), genes related to cholesterol synthesis, pharmacological treatments that alter lipid metabolism and the possible participation in suicidal behavior. Nevertheless, future research is required to describe how serum cholesterol affects cholesterol metabolism in the CNS to establish and understand the role of cholesterol in suicidal behavior.

Eating disorders are psychiatric disorders characterized by disturbed eating behaviors. They have a complex etiology in which genetic and environmental factors interact. Analyzing gene-environment interactions could help us to identify the mechanisms involved in the etiology of such conditions. For example, comethylation module analysis could detect the small effects of epigenetic interactions, reflecting the influence of environmental factors. We used MethylationEPIC and Psycharray microarrays to determine DNA methylation levels and genotype from 63 teenagers with eating disorders. We identified 11 comethylation modules in WGCNA (Weighted Gene Correlation Network Analysis) and correlated them with single nucleotide polymorphisms (SNP) and clinical features in our subjects. Two comethylation modules correlated with clinical features (BMI and height) in our sample and with SNPs associated with these phenotypes. One of these comethylation modules (yellow) correlated with BMI and rs10494217 polymorphism (associated with waist-hip ratio). Another module (black) was correlated with height, rs9349206, rs11761528, and rs17726787 SNPs, these polymorphisms were associated with height in previous GWAS. Our data suggest that genetic variations could alter epigenetics, and that these perturbations could be reflected as variations in clinical features.

Schizophrenia is a common, chronic and debilitating neuropsychiatric syndrome affecting tens of millions of individuals worldwide. While rare genetic variants play a role in the etiology of schizophrenia, most of the currently explained liability is within common variation, suggesting that variation predating the human diaspora out of Africa harbors a large fraction of the common variant attributable heritability. However, common variant association studies in schizophrenia have concentrated mainly on cohorts of European descent. We describe genome-wide association studies of 6152 cases and 3918 controls of admixed African ancestry, and of 1234 cases and 3090 controls of Latino ancestry, representing the largest such study in these populations to date. Combining results from the samples with African ancestry with summary statistics from the Psychiatric Genomics Consortium (PGC) study of schizophrenia yielded seven newly genome-wide significant loci, and we identified an additional eight loci by incorporating the results from samples with Latino ancestry. Leveraging population differences in patterns of linkage disequilibrium, we achieve improved fine-mapping resolution at 22 previously reported and 4 newly significant loci. Polygenic risk score profiling revealed improved prediction based on trans-ancestry meta-analysis results for admixed African (Nagelkerke’s R2 = 0.032; liability R2 = 0.017; P −52), Latino (Nagelkerke’s R2 = 0.089; liability R2 = 0.021; P −58), and European individuals (Nagelkerke’s R2 = 0.089; liability R2 = 0.037; P −113), further highlighting the advantages of incorporating data from diverse human populations.

Genetic factors have been implicated in suicidal behavior. It has been suggested that one of the roles of genetic factors in suicide could be represented by the effect of genetic variants on gene expression regulation. Alteration in the expression of genes participating in multiple biological systems in the suicidal brain has been demonstrated, so it is imperative to identify genetic variants that could influence gene expression or its regulatory mechanisms. In this study, we integrated DNA methylation, gene expression, and genotype data from the prefrontal cortex of suicides to identify genetic variants that could be factors in the regulation of gene expression, generally called quantitative trait locus (xQTLs). We identify 6,224 methylation quantitative trait loci and 2,239 expression quantitative trait loci (eQTLs) in the prefrontal cortex of suicide completers. The xQTLs identified influence the expression of genes involved in neurodevelopment and cell organization. Two of the eQTLs identified (rs8065311 and rs1019238) were previously associated with cannabis dependence, highlighting a candidate genetic variant for the increased suicide risk in subjects with substance use disorders. Our findings suggest that genetic variants may regulate gene expression in the prefrontal cortex of suicides through the modulation of promoter and enhancer activity, and to a lesser extent, binding transcription factors.

Resumen La neurociencia y la neurotecnologia actuales han permitido un mayor conocimiento de presuntos sustratos y mecanismos involucrados en emociones, conductas, pensamientos y en la toma de decisiones morales. El uso de estas herramientas plantea preocupaciones sobre el posible mal uso, o incluso sobreuso, de la manipulacion cerebral. La neuroetica es la disciplina dedicada a estudiar estos temas. La neuroetica en Mexico se encuentra en una etapa naciente, por lo que se sugiere cautela en temas no reportados en la literatura internacional como factores medicos (por ejemplo, medicina prehispanica), legales (por ejemplo, marcos ambiguos en neurociencia y neurotecnologia) y socioculturales (por ejemplo, etnografia, mezcla de filosofia del oeste y prehispanicas), por lo que es necesaria una reflexion con el objetivo de enfocarse en: a) el bien del paciente en un contexto cultural mexicano y b) fomentar una neuroetica global, considerando la diversidad cultural neurocognitiva dentro de un marco de respeto etnografico.

Background Circulating cell-free mitochondrial DNA (cf-mtDNA) fragments in blood plasma have been reported in patients with schizophrenia (SZ). Although the relationship of cf-mtDNA to the cognitive status of patients with SZ has not yet been explored, it is known that cognitive impairment in SZ compromises the functional and social capacity of these patients and diminishes their quality of life. In this sense, the assessment of the severity of cognitive impairment in a Mexican population with SZ and its association with cf-mtDNA levels in blood plasma may provide the possibility of using cf-mtDNA as a biomarker to determine the status of the disease and the possible ensuing changes over time. Methods Subjects for a case-control study will be recruited. cf-mtDNA obtained from blood plasma will be quantified by real-time polymerase chain reaction, using melting curve technology with SYBR green as amplification marker. Patients with SZ will be grouped into those with severe, mild, and no cognitive impairment according to Montreal Cognitive Assessment scale scores, to determine differences between cognitive performance and cf-mtDNA levels in blood plasma. Ethics and communication This study has been approved by the ethics and investigation committees of the High Specialty Regional Hospital of Mental Health (Hospital Regional de Alta Especialidad de Salud Mental); project No. HRAESM/DG/RP/1128/2018. We plan to communicate our research findings in scientific conferences and in peer-reviewed journals. Conclusion It is known that cognitive dysfunction provokes negative effects in an SZ patient´s life. This project aims to provide better knowledge about the role of cf-mtDNA in the pathogenesis of cognitive impairment in SZ, as an attempt to achieve improvements to the existing treatments, thereby helping to prevent major cognitive deterioration.

Adverse conditions in early life, including environmental, biological and social influences, are risk factors for ill-health during aging and the onset of age-related disorders. In this context, the recent field of social epigenetics offers a valuable method for establishing the relationships among them However, current clinical studies on environmental changes and lifespan disorders are limited. In this sense, the Tlaltizapan (Mexico) cohort, who 52 years ago was exposed to infant malnutrition, low income and poor hygiene conditions, represents a vital source for exploring such factors. Therefore, in the present study, 52 years later, we aimed to explore differences in clinical/biochemical/anthropometric and epigenetic (DNA methylation) variables between individuals from such a cohort, in comparison with an urban-raised sample. Interestingly, only cholesterol levels showed significant differences between the cohorts. On the other hand, individuals from the Tlaltizapan cohort with more years of schooling had a lower epigenetic age in the Horvath (p-value = 0.0225) and PhenoAge (p-value = 0.0353) clocks, compared to those with lower-level schooling. Our analysis indicates 12 differentially methylated sites associated with the PI3-Akt signaling pathway and galactose metabolism in individuals with different durations of schooling. In conclusion, our results suggest that longer durations of schooling could promote DNA methylation changes that may reduce epigenetic age, nevertheless, further studies are needed.

The aim of this study was to explore the knowledge, emotions and perceived stressors by healthcare workers who were in contact with infected patients during the COVID-19 outbreak. An online cross-sectional survey was applied. Data were collected from N = 263 healthcare workers in Tabasco State, Mexico. We developed and administered a questionnaire, which consisted of sociodemographic characteristics, plus four sections. The sections evaluated were (1) knowledge of COVID-19, (2) feelings/emotions during the COVID-19 outbreak, (3) factors that caused stress and (4) factors that helped to reduce stress. Surveyed individuals were divided into three groups: physicians, nurses and other healthcare workers. When we evaluated their knowledge of COVID-19 we observed that the majority of healthcare workers in the three groups reported that they knew about COVID-19. Physicians indicated that they felt insecure about practicing their profession (62.5%) due to the high risk of being in contact with SARS-CoV-2. With regards to stressor factors, the risk of transmitting COVID-19 to their families was the main factor causing moderate to high stress (95.4%). Finally, we found that “your profession puts your life at risk” was the only factor associated with feeling nervous and scared (PR: 3.15, 95% CI: 1.54–6.43). We recommended health education campaigns, introductory courses on COVID-19 and other infectious diseases, management protocols and the provision of protection equipment to health workers in order to reduce personal and professional fears of contagion and to improve the health system in Mexico when facing epidemics.

The combination of substance use and psychiatric disorders is one of the most common comorbidities. The objective of this study was to perform a genome-wide association study of this comorbidity (Com), substance use alone (Subs), and psychiatric symptomatology alone (Psych) in the Mexican population. The study included 3914 individuals of Mexican descent. Genotyping was carried out using the PsychArray microarray and genome-wide correlations were calculated. Genome-wide associations were analyzed using multiple logistic models, polygenic risk scores (PRSs) were evaluated using multinomial models, and vertical pleiotropy was evaluated by generalized summary-data-based Mendelian randomization. Brain DNA methylation quantitative loci (brain meQTL) were also evaluated in the prefrontal cortex. Genome-wide correlation and vertical pleiotropy were found between all traits. No genome-wide association signals were found, but 64 single-nucleotide polymorphism (SNPs) reached nominal associations (p Subs-PRS, Com-PRS, and Psych-PRS) were associated with all of the traits. Brain meQTL of the Subs-associated SNPs had an effect on the genes enriched in insulin signaling pathway, and that of the Psych-associated SNPs had an effect on the Fc gamma receptor phagocytosis pathway.