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Theory My severe autism is slowly killing my brain's critical thinking abilities.

Scilence

Scilence

Hail Satan
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Joined
Feb 18, 2022
Posts
207
First and foremost, my prefrontal cortex likely never fully developed and probably mutated from single wage slave bad english mother plus siblings moved out. In addition, she was a fairly old mother who likely consumed much lead and microplastics plus had sinking uterus organs. And, then as a result of that, any social interaction I partake in usually have me overanalysing and overremembering them for often weeks and hours at a time. Some theories stipulate autism is a protective mechanism for people who have been alone for a long time to prevent random strangers from stealing from us/ killing us, by maximizing our attention spans to them. Thus, whatever they do will be permanently scarred in my head for the next few weeks/ months. Also, because my prefrontal cortex is deformed, I most likely have to use my critical thinking capabilities to engage in any social interactions be it body language or speaking. Thus, it is over for me and I must go into hiding.
 
u probably have zero critical thinking and ur just a dumb ass who think he smart
 
u probably have zero critical thinking and ur just a dumb ass who think he smart
I have always thought that way too, since my brain is likely also deformed in general.
 
its mostly over if your not NT . :feelsclown:

Ofc Chad sint affected by this , unless hes Hyper Tistic "
 
welcome to early dementia club
 
My brother is like that, he overcomplicate and over analyze simple thing and he can never make an decision, he spends days and week to decide between something.
 
u probably have zero critical thinking and ur just a dumb ass who think he smart
From reading this post, it's definitely the latter
 
welcome to early dementia club

No, not quite.

Senile plaques (SP) and neurofibrillary tangles (NFT) are the major histopathological changes that occur in Alzheimer's disease (AD). How these two different types of lesions are related to each other and to the dementia of AD is unknown. Recent studies lead to paradoxical conclusions: NFT and neuronal alterations such as synapse loss are much more closely related to the symptoms of dementia than are SP. However, mutations in the beta-amyloid protein of SP have been found in some patients with familial AD, suggesting that an abnormality in amyloid causes the development of SP, NFT and AD dementia. Examination of transgenic animals that produce amyloid precursor protein (APP), or altered forms of APP, may lead to the development of an animal model of AD, and ultimately to answers that link amyloid production to neuronal alterations, and cognitive impairments.

Now...APBA1 demonstrated by my variant will help us reach the next phase:

Sniecker



Sniek



www.ncbi.nlm.nih.gov
www.ncbi.nlm.nih.gov
PopulationGroupSample SizeRef AlleleAlt Allele

PopulationGroupSample SizeRef AlleleAlt Allele
Total Global10618G=0.59314A=0.40686, T=0.00000
European Sub8276G=0.5168A=0.4832, T=0.0000
African Sub1406G=0.9587A=0.0413, T=0.0000
African Others Sub54G=0.94A=0.06, T=0.00
African American Sub1352G=0.9593A=0.0407, T=0.0000
Asian Sub46G=0.91A=0.09, T=0.00
East Asian Sub32G=0.88A=0.12, T=0.00

Many of the implicated genes are involved in neuronal function: DCC, APBA1, PRR7, ZFHX3, HCRTR1, NEGR1, MEF2C, SHANK3 and ATXN2L (see Supplementary Note for the GeneCards summaries).

In conclusion, we conducted a meta-analysis GWAS and GWGAS for intelligence, including 13 cohorts and 78,308 individuals. We confirmed three loci and 12 genes, and identified 15 novel genomic loci and 40 novel genes for intelligence. Pathway analysis demonstrated the involvement of genes regulating cell development. We showed genetic overlap with several neuropsychiatric and metabolic disorders. These findings provide starting points for understanding the molecular neurobiological mechanisms underlying intelligence, one of the most investigated traits in humans

rs11138902APBA1 intronic9q21.11ag0.545.494.12E-08+++++-++783071

Clearly, APBA1 is closely associated with intelligence.
Intelligence has been associated with many socio-economic and health-related outcomes. We used whole-genome LD Score Regression12 to calculate the genetic correlation with 32 traits from these domains for which GWAS summary statistics were available for download. Significant genetic correlations were observed with 14 traits. The strongest, positive genetic correlation was with Educational attainment (rg=0.70, SE=0.02, P=2.5×10−287). Moderate, positive genetic correlations were observed with smoking cessation, intracranial volume, head circumference in infancy, Autism spectrum disorder and height. Moderate negative genetic correlations were observed with Alzheimer’s disease, depressive symptoms, having ever smoked, schizophrenia, neuroticism, waist-to-hip ratio, body mass index, and waist circumference (Fig. 3d; Supplementary Table 13).
 

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