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Is it over for all schizo

Eminemshalfbrother

Eminemshalfbrother

Officer
★★★
Joined
Dec 26, 2023
Posts
786
Does having schizophrenia automatically mean it’s over? The stigma around people with schizophrenia is insane, like holyyyyy shieet. It’s not like you gotta tell them too, they fucking notice no matter how normal you act, they smell it, even if they don’t assume your schizophrenic, they will walk away from any interaction thinking “what’s wrong with that guy?” So do you guys think having schizophrenia mean it’s over no matter what?
 
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TCF4


Individuals with disorders that include psychotic symptoms (i.e. psychotic disorders) experience broad cognitive impairments in the chronic state, indicating a dimension of abnormality associated with the experience of psychosis. These impairments negatively impact functional outcome, contributing to the disabling nature of schizophrenia, bipolar disorder, and psychotic depression. The robust and reliable nature of cognitive deficits has led researchers to explore the timing and profile of impairments, as this may elucidate different neurodevelopmental patterns in individuals who experience psychosis. Here, we review the literature on cognitive deficits across the life span of individuals with psychotic disorder and psychotic-like experiences, highlighting the dimensional nature of both psychosis and cognitive ability. We identify premorbid generalized cognitive impairment in schizophrenia that worsens throughout development, and stabilizes by the first-episode of psychosis, suggesting a neurodevelopmental course.

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


Schizo
 
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