16 Matching Annotations
  1. Nov 2025
    1. Genes related to stress response, such as FKBP5 gene

      Side Note: FKBP5 gene is unlike the taster gene that we looked at where it is known to be for "tasting," rather this gene is "related to stress response" which goes to show that Schizophrenia is likely onset by traumatically stressful events.

    2. Lower meth-ylation status has been observed in patients withfirst-episode psychosis reporting traumatic ex-periences

      If less methylated, this means that the DNA is more accessible for transcription, which would allow the gene to be expressed more. In this case, if these genes are what causes schizophrenia, less methylation is extremely bad for patients.

    3. The FKBP5 rs9296158, rs4713916, rs992105 andrs3800373 SNPs have been found to be irrele-vant in the association between childhood trau-ma and cognitive functioning in patients withpsychotic disorder

      Perhaps these SNPs are silent based on when they are transcribed, meaning when the trauma happens depends on whether or not the SNP is in transcription and then reflected in translation?

    4. The T allele of SNP rs1360780 andA alleles for SNPs rs9296158 and rs1043805 in-teracting with childhood trauma have been in-dicated as significant risk factors of subclini-cal psychosis in general twin population

      How/Why would a specific allele have more of a significant risk for people of the twin population? Would it be because of how they are in-utero or possibly because of the split egg for identical twins?

    5. Increased risk of schizo-phrenia development has been observed in car-riers of risk G allele in rs3800373 SNP of FKBP5gene after accounting for childhood trauma

      What about carriers of the risk G allele without accounting for childhood trauma?

    6. Higher peripheral FKBP5 mRNA lev-els have been observed in people with schiz-ophrenia when compared to healthy controls

      Would higher mRNA levels indicate that there are too many of the transcription factors present in the body that make transcription happen too much?

    7. food deprivation in micehave been found to result in increased FKBP5expression

      If something like food deprivation increases FKBP5 gene expressions, which is hypothesized to make someone more susceptible to schizophrenia, this would presumably make people in lower income areas more prone to getting schizophrenia. Possibly why homeless people have a higher ratio of people with mental illness compared to people who have homes?

    8. Cortisol level may also im-pact a symptomatic severity. It has been report-ed that increased salivary cortisol level positive-ly correlates with negative symptoms severity

      Even though cortisol may not be the cause of forms of psychosis or more particularly schizophrenia, it does correlate with how severe symptoms are which is very interesting. Maybe something else is the on/off switch for the disease, while cortisol acts as an amplifier?

    9. Cortisol acts through its cytoplas-mic glucocorticoid receptor (GR) that is translo-cated to the nucleus after its activation. The GRis acting as a transcription factor which can bindto specific DNA sequences and thus regulate thetranscriptional response to stress

      Given that cortisol has a glucocorticoid receptor (GR), the receptor is likely membrane impermeable.

      Since the GR acts as a transcription factor, transcription of certain DNA would be severely impacted of the transcription factor were not present because it would not be able to effectively carry out the function in an efficient manner.

    10. terioration of cognitive functioning [16-18] exac-erbations of the disease and increased intensityof both positive and negative symptoms

      Note: include the first part of this sentence too (I could not because of formatting for some reason)

      This is extremely interesting because the body has its own signaling and response systems within the body that happen subconsciously such as releasing cortisol. Does this lead to signs that cortisol is in fact bad for us and causing mental diseases such as Schizophrenia? If so, would there even be a fix given that this is something that the body produces on its own?

    1. Dysregulation of the HPA in disease is likely a product of inappropriate checks and balances betweenexcitatory and inhibitory inputs ultimately impacting PVN output

      Pretty sure the inhibition of FKBF5 gene in schizophrenia is what causes the HPA axis dysregulation in patients that experience schizophrenia relative to the specific gene.

      **Check with original review article **

    2. Inhibition of stressor-evoked HPA axis responses is mediatedby an elaborate network of glucocorticoid receptor (GR)-containing circuits, providing a distributednegative feedback signal that inhibits PVN neurons

      connection to lecture about cell signaling and negative feedback inhibition of gene expression

    3. Amygdala subnuclei drive HPA axis responses indirectly viadisinhibition, mediated by GABAergic relays onto PVN-projecting neurons in the hypothalamus andbed nucleus of the stria terminalis (BST).

      How the HPA axis is operated