Leave these fields empty (spam trap):
Name
You can leave this blank to post anonymously, or you can create a Tripcode by using the float Name#Password
Comment
[*]Italic Text[/*]
[**]Bold Text[/**]
[~]Taimapedia Article[/~]
[%]Spoiler Text[/%]
>Highlight/Quote Text
[pre]Preformatted & Monospace text[/pre]
1. Numbered lists become ordered lists
* Bulleted lists become unordered lists
File

Sandwich


Netjester is chatting 24/7 on Twitch and channel subscribers can use his emoticon
Psychotic thought that the schizo-gene shared is trial/error adaptation by Basil Hinningshit - Sun, 15 Apr 2018 03:20:09 EST ID:dSA4F4Wp No.55373 Ignore Report Quick Reply
File: 1523776809371.jpg -(42378B / 41.38KB, 540x304) Thumbnail displayed, click image for full size. 42378
Any brain scientists, Psych doctors and DNA coders lurking humor this thought?


I'm schizophrenic in midst of psychosis, I've believed to have figured out from a binge watch on schizophrenia docs i've used as white noise, that i've mapped out the cause of schizophrenia

In the part of the brain where the input/output ratio is processed. out processors send out mixed signals causing us to chain into constant misunderstood {cause} = misfired {effect} (causing a blunt affect too)
I think the gene that causes that misfire of reactions to one's perception is the trial and error program written into our DNA meant to test adaptability by making it so that one's perception and cognitive reaction to be mixed matched from each other in order to promote adaptability to unplanned reactions. it's a survival tool gone....insane
>>
A_Wizard !cMZsY.BCnU!!vVWR8L52 - Mon, 16 Apr 2018 02:48:09 EST ID:p98oIwAn No.55375 Ignore Report Quick Reply
>>55373
That's a sound theory, though I can't test the DNA aspect myself. I'm too high and tired to really aid you directly at the moment, but I will suggest reading some classic texts that give good examples of thought analysis. http://www.sacred-texts.com/cla/plato/apology.htm
Also, by tracing your thoughts back to their origin, periodically throughout the day (especially when a thought seems weird), the practice will help you understand the methods involved in the thought processes as well as make you more consciously aware of them. This in turn will help get onto a path where you will learn to script your own thought processes and turn on and off various processes or throttle sensory input, as to allow better processing.
>>
Fucking Nummerstork - Tue, 17 Apr 2018 05:44:17 EST ID:seInJVW2 No.55377 Ignore Report Quick Reply
>where the input/output ratio is processed

Glutaminergic signalling

>In order to support the localization hypothesis, it would be necessary to show differing cellular signaling pathways are activated by NMDA receptors based on its location within the cell membrane.[39] Experiments have been designed to stimulate either synaptic or non-synaptic NMDA receptors exclusively. These types of experiments have shown that different pathways are being activated or regulated depending on the location of the signal origin.[44] Many of these pathways use the same protein signals, but are regulated oppositely by NMDARs depending on its location. For example, synaptic NMDA excitation caused a decrease in the intracellular concentration of p38 mitogen-activated protein kinase (p38MAPK). Extrasynaptic stimulation NMDARs regulated p38MAPK in the opposite fashion, causing an increase in intracellular concentration.[45][46] Experiments of this type have since been repeated with the results indicating these differences stretch across many pathways linked to cell survival and excitotoxicity.[39]

>out processors send out mixed signals causing us to chain into constant misunderstood {cause} = misfired {effect} (causing a blunt affect too)

Breakdown of the kynurenine pathway of tryptophan's metabolism.

>A recent study shows that a genetic variation resulting in decreased expression of SNX7 is linked to increased central levels of kynurenic acid and ultimately to psychosis and cognitive dysfunction in bipolar disorder

>We conducted a genome-wide association study (GWAS) against CSF levels of KYNA in BD that revealed a genome-wide significant association with the single-nucleotide polymorphism (SNP) rs10158645 within 1p21.3, a finding that was replicated in an independent cohort of BD patients.

>I think the gene that causes that misfire of reactions to one's perception is the trial and error program written into our DNA meant to test adaptability by making it so that one's perception and cognitive reaction to be mixed matched from each other in order to promote adaptability to unplanned reactions.

>Research is done on 10–12 genes on 1q21.1 that produce DUF1220-locations. DUF1220 is an unknown protein, which is active in the neurons of the brain near the neocortex. Based on research on apes and other mammals, it is assumed that DUF1220 is related to cognitive development (man: 212 locations; chimpanzee: 37 locations; monkey: 30 locations; mouse: 1 location). It appears that the DUF1220-locations on 1q21.1 are in areas that are related to the size and the development of the brain. The aspect of the size and development of the brain is related to autism (macrocephaly) and schizophrenia (microcephaly). It has been proposed that a deletion or duplication of a gene that produces DUF1220-areas might cause growth and development disorders in the brain [12]

>Results of this research demonstrate that DUF1220 copy number is linearly associated with increased cognitive function as measured by total IQ and mathematical aptitude scores, a finding identified in two independent populations.[13][19]. This association has important implications for understanding the interplay between cognitive function and autism phenotypes.[20] These findings also provide additional support for the involvement of DUF1220 in a genomic trade-off model involving the human brain: the same key genes that have been major contributors to the evolutionary expansion of the human brain and human cognitive capacity may also, in different combinations, underlie psychiatric disorders such as autism and schizophrenia. [14]

1p21 variations leading to underactive NMDAR activity triggering a build up of toxic tryptophan byproducts that permanently inhibit the NMDA receptors affixed to dopamine neurons which leads to hyperfiring of dopamine neurons and the positive syndrome of psychosis (also implicated in affective disorders). Chronic disinhibition of glutaminergic firing leads to negative syndrome. The brain attempts to correct for this by elevating levels of kynurenic acid as kynurenic acid is neuroprotective but it cannot correct for terminal endings that have already been damaged which is why intervention during the first episode of psychosis is so conductive to good functioning. The more one stays in the psychotic state the more damage is inflicted upon the NMDA and thus the more one enters further psychosis as a result.


Report Post
Reason
Note
Please be descriptive with report notes,
this helps staff resolve issues quicker.