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Mental Illnesses Do not exist!

S

SUPREMECOMMANDER

Banned
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Mar 18, 2023
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Kill yourself you nigger faggot
 
Sorry OP you are severely mentally ill
 
Take your meds!
 
I have ASD coupled with schizotypal traits.

Schizotypal personality disorder is an ingrained pattern of thinking and behavior marked by unusual beliefs and fears, and difficulty with forming and maintaining relationships. This disorder is within the schizophrenia spectrum.
People with schizotypal personality disorder are uncomfortable with close relationships and may exhibit eccentric behavior. Speech may include digressions, odd use of words, or evidence of magical thinking, such as a belief in clairvoyance and bizarre fantasies. Patients usually experience distorted thinking and avoid intimacy. They typically have few, if any, close friends, and feel nervous around strangers although they may marry and maintain jobs. The disorder, which may appear more frequently in males, surfaces by early adulthood and can exacerbate anxiety and depression.
Schizotypal personality disorder is classified under the Diagnostic and Statistical Manual of Mental Disorders-5. Cluster A is described as odd, eccentric. The other two cluster A personality disorders are schizoid personality disorder and paranoid personality disorder. Social awkwardness and withdrawal are hallmarks of this cluster.

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...

NINDS : 52 Autistic disorder (sometimes called autism or classical ASD) is the most common condition in a group of developmental disorders known as the autism spectrum disorders (ASDs). Autistic children have difficulties with social interaction, display problems with verbal and nonverbal communication, and exhibit repetitive behaviors or narrow, obsessive interests. These behaviors can range in impact from mild to disabling. Autism varies widely in its severity and symptoms and may go unrecognized, especially in mildly affected children or when more debilitating handicaps mask it. Scientists aren’t certain what causes autism, but it’s likely that both genetics and environment play a role. Autism spectrum disorder is diagnosed based on symptoms, signs, and other testing according to the Diagnostic and Statistical Manual V, a guide created by the American Psychiatric Association to diagnose mental disorders. Children should be screened for developmental delays during periodic checkups and specifically for autism at 18- and 24-month well child visits.




TCF4




The Psychiatric Risk Gene Transcription Factor 4 (TCF4) Regulates Neurodevelopmental Pathways Associated With Schizophrenia, Autism, and Intellectual Disability​

Genetic variants in and around the transcription factor 4 (TCF4) gene are associated with range of disorders that are frequently associated with cognitive dysfunction.1–3 The most recent schizophrenia GWAS reported three independent single nucleotide polymorphisms (SNPs) in TCF4 that surpassed the threshold for genome wide significance.4 Intriguingly, rare TCF4 single nucleotide variants (SNVs) have also been described in schizophrenia patients, although their impact on the function of the protein has not been established.5,6 In addition to the genetic studies in schizophrenia, TCF4 variants are associated with early information processing and cognitive markers, some of which are schizophrenia endophenotypes.7–10 Damaging TCF4 mutations have also been described in large-scale genotyping studies in patients with ID, neurodevelopmental disorders, and most recently ASD.11–15 Haploinsufficiency of TCF4 causes Pitt–Hopkins syndrome (PTHS); a rare form intellectual disability (ID) associated with characteristic facial features, autonomic dysfunction, and behavioral traits that resemble autism spectrum disorder (ASD).16–19 Collectively, these studies implicate TCF4 in a range of neurodevelopmental disorders.

CF4 is a member of the basic helix-loop-helix (bHLH) family of proteins.20–22 For the purposes of disambiguation, it should be noted that TCF4 (Gene ID: 6925) described herein should not be confused with T-cell factor 4 (Gene ID: 6934, official gene symbol, TCF7L2) since they can share the same acronym. TCF4 and its paralogues, collectively known as E-proteins, interact with other bHLH proteins to regulate DNA binding specificity and transcriptional activity at promoters and enhancers that contain E-boxes (5′-CANNTG).2,20,23 The human TCF4 gene encodes multiple protein isoforms of which only the major isoforms TCF4-A and TCF4-B have been characterized in detail.24 In neurons, TCF4 regulates the intrinsic excitability of pyramidal cells of the prefrontal cortex and has been shown to attenuate neurite branching.25,26 Furthermore, haploinsufficiency of Tcf4 in mice affects gene expression and DNA methylation in the brain, leading to enhanced long-term potentiation, learning and memory deficits, and autistic-like behavior.22,25,26 By contrast, mice over-expressing Tcf4 in the brain display deficits in sensorimotor gating, fear conditioning, and circadian processes as well as impairments in attentional and behavioral anticipation.7,27

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Converging evidence for a pseudoautosomal cytokine receptor gene locus in schizophrenia​

Schizophrenia is a strongly heritable disorder, and identification of potential candidate genes has accelerated in recent years. Genomewide scans have identified multiple large linkage regions across the genome, with fine-mapping studies and other investigations of biologically plausible targets demonstrating several promising candidate genes of modest effect. The recent introduction of technological platforms for whole-genome association (WGA) studies can provide an opportunity to rapidly identify novel targets, although no WGA studies have been reported in the psychiatric literature to date. We report results of a case-control WGA study in schizophrenia, examining approximately 500 000 markers, which revealed a strong effect (P=3.7 x 10(-7)) of a novel locus (rs4129148) near the CSF2RA (colony stimulating factor, receptor 2 alpha) gene in the pseudoautosomal region. Sequencing of CSF2RA and its neighbor, IL3RA (interleukin 3 receptor alpha) in an independent case-control cohort revealed both common intronic haplotypes and several novel, rare missense variants associated with schizophrenia. The presence of cytokine receptor abnormalities in schizophrenia may help explain prior epidemiologic data relating the risk for this illness to altered rates of autoimmune disorders, prenatal infection and familial leukemia.

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Further evidence that the rs1858830 C variant in the promoter region of the MET gene is associated with autistic disorder​


Pamela B Jackson 1 , Luigi Boccuto, Cindy Skinner, Julianne S Collins, Giovanni Neri, Fiorella Gurrieri, Charles E Schwartz

Affiliations



Abstract​


Previous studies in three independent cohorts have shown that the rs1858830 C allele variant in the promoter region of the MET gene on chromosome 7q31 is associated with autism. Another study has found correlations between other alterations in the MET gene and autism in two unrelated cohorts. This study screened two cohorts, an Autistic Disorder cohort from South Carolina and a Pervasive Developmental Disorder (PDD) cohort from Italy, for the presence of the C allele variant in rs1858830. A significant increase in the C allele variant frequency was found in the South Carolina Autistic Disorder patients as compared to South Carolina Controls (chi(2)=5.8, df=1, P=0.02). In the South Carolina cohort, a significant association with Autistic Disorder was found when comparing the CC and CG genotypes to the GG genotype (odds ratio (OR)=1.64; 95% confidence interval (CI)=1.12-2.40; chi(2)=6.5, df=1, P=0.01) in cases and controls. In the Italian cohort, no significant association with PDD was found when comparing the CC or CG genotype to the GG genotype (OR=1.20; 95% CI=0.56-2.56; chi(2)=0.2, df=1, P=0.64). This study is the third independent study to find the rs1858830 C variant in the MET gene promoter to be associated with autism.

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6


Systemizing is genetically correlated with autism and is genetically distinct from social autistic traits​



Abstract​

The hypersystemizing theory of autism suggests that autistic individuals, on average, have superior attention to detail, and a stronger drive to systemize. Systemizing involves identifying input-operation-output relationships. Here, we report the results of genome-wide association studies (GWAS) of systemizing measured using the Systemizing Quotient - Revised in n = 51,564 individuals. We identify three genome-wide significant loci: Two of these were significant in the non-stratified GWAS: rs4146336 on chromosome 3 (P = 2.58×10−8) and rs1559586 on chromosome 18 (P = 4.78×10−8). In addition, we also identified a significant locus in the males-only GWAS (rs8005092 on chromosome 14, P = 3.74×10−8). We find that 12%± 1.2 of the variance in systemizing is captured by SNPs (P=1.2×10−20). We identify a positive genetic correlation between autism and systemizing (rg = 0.26±0.06; P = 3.35×10−5), which is independent of genetic contribution to educational attainment. We further demonstrate that genetic risk for autism from systemizing is genetically distinct from genetic risk emerging from social autistic traits, suggesting distinct shared genetics between autism and social and non-social traits. Our results highlight the importance of considering both social and non-social autistic traits in elucidating the genetic architecture of autism.

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