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Theory IQ and Genes

Intellau_Celistic

Intellau_Celistic

5'3 KHHV Mentalcel
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IQ is mostly determined by genetics, though environmental factors such as stress and nutrition can also play a role...

Terms:

-IQ (Intelligence Quotient)

-FSIQ(Full Scale IQ)

-VIQ(Verbal IQ)

-PIQ(Performance IQ)

Terms may vary across IQ tests. Also, different tests measure different aspects of IQ.

sample Result:

1647515282270


Above we see a "High Average" verbal Working Memory(WM) on the Stanford-Binet IQ scale. His Nonverbal Fluid Reasoning, though, is low average.

This is further explained by a simple academic achievement test(WIAT):

1647515430296


And of-course, the WIAT is highly correlated with IQ scales:

Briefly, the WISC–IV is used to assess general thinking and reasoning skills of children aged 6 years to 16 years. This test has five main areas that are; Verbal Comprehension Index (VCI), Perceptual Reasoning Index (PRI), Working Memory Index (WMI), Processing Speed Index (PSI), and Full Scale scores.

On the other hand, the WIAT-II is an achievement test for individuals ages four through adulthood. Skills that are tested are Reading (Word Reading, Reading Comprehension, Pseudo word Decoding); Mathematics (Numerical Operations, Mathematics Reasoning); Written Language (Spelling, Written Expression); and Oral Language (Listening Comprehension, Oral Expression).

There is a rather high correlation between the WISC-IV and WIAT-II at the composite level. The VCI is highly correlated with Reading and Oral
Language, the PRI is highly correlated with Math, WMI is highly correlated with Reading, and PSI is highly correlated to Written Language. With the rather high correlation, the scores of the boy you are dealing with do not match.
(http://www.brainy-child.com/experts/WISC-IV-WIAT-scores.shtml)

1647515883772

(High correlation between the WISC scale and the Stanford-Binet Scale)

Below we discuss several IQ-related genes. I'll offer a map to represent global representative populations...

HapMap


Now, we will look at the "WWC1" gene. This gene is associated with Working Memory of both verbal and performance.

This is my sample:

Memory

(A variant common among East Asian populations...)

Association of KIBRA with episodic and working memory: a meta-analysis
WWC1 was first implicated in human cognition through a genome wide association study in 2006 that reported an association of the intronic single nucleotide polymorphism (SNP) rs17070145 with episodic memory performance. WWC1 encodes the protein KIBRA, which is almost ubiquitously expressed. Together with its binding partners, KIBRA is assumed to play a role in synaptic plasticity. T-allele carriers of SNP rs17070145 have been reported to outperform individuals that are homozygous for the C-allele in episodic memory tasks. Here we report two random effects meta-analyses testing the association of rs17070145 with episodic and working memory. All currently available population-based association studies that investigated effects of rs17070145 on episodic or working memory were included in the analyses. Where performance measures for multiple domain-specific tasks were available for a given study population, averaged effect size estimates were calculated. The performed meta-analyses relied on 17 samples that were tested for episodic memory performance (N = 8,909) and 9 samples that had performed working memory tasks (N = 4,696). We report a significant association of rs17070145 with both episodic (r = 0.068, P = 0.001) and working memory (r = 0.035, P = 0.018). In summary, our findings indicate that SNP rs17070145 located within KIBRA explains 0.5% of the variance for episodic memory tasks and 0.1% of the variance for working memory tasks in samples of primarily Caucasian background.​



KIBRA: A New Gateway to Learning and Memory?​

Armin Schneider,1,* Matthew J. Huentelman,2 Joachim Kremerskothen,3 Kerstin Duning,3 Robert Spoelgen,1 and Karoly Nikolich4,*
Author information Article notes Copyright and License information Disclaimer
This article has been cited by other articles in PMC.

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Abstract​

The genetic locus encoding KIBRA, a member of the WWC family of proteins, has recently been shown to be associated with human memory performance through genome-wide single nucleotide polymorphism screening. Gene expression analysis and a variety of functional studies have further indicated that such a role is biologically plausible for KIBRA. Here, we review the existing literature, illustrate connections between the different lines of evidence, and derive models based on KIBRA's function(s) in the brain that can be further tested experimentally.
Keywords: cognition, memory, hippocampus, genome-wide association study (GWAS), Alzheimer's disease, cognitive impairment, PKCζ

KIBRA has come into the focus of the neurogenetics field following the publication of human evidence pointing to an involvement of the gene in memory performance and cognition (Papassotiropoulos et al., 2006). In that publication, the authors report that carriers of the KIBRA/ WWC1 (rs17070145) T allele or, to a lesser extent, the calsyntenin 2 (CLSTN2) rs6439886 T allele performed significantly better on multiple episodic memory tasks than those homozygous for the C allele at either polymorphism. Furthermore, using functional magnetic resonance imaging (fMRI), they observed that brain activation (measured as oxygen extraction from blood) in key areas associated with memory retrieval was significantly greater in a selection of 15 WWC1 (rs17070145) T-allele-noncarriers than in 15 T-allele-carriers during an episodic memory task. After this initial finding, a considerable number of studies examined the WWC1 polymorphism in different contexts of cognition and in different populations (summarized in Table Table11 and reviewed below).

KIBRA is predominately expressed in the kidney and brain in the adult organism. In the rodent and human brain, KIBRA is expressed in memory-related structures (including the hippocampus and cortex), the cerebellum, and in the hypothalamus (Johannsen et al., 2008). During brain development, expression has been shown to decrease from juvenile postnatal stages to the adult animal (Johannsen et al., 2008). On a subcellular level within neurons, KIBRA shows a somatodendritic staining pattern with enrichment in the perinuclear region and in postsynaptic structures. In subcellular fractionation experiments, KIBRA was heavily enriched in the postsynaptic density (PSD) fraction (Johannsen et al., 2008). However, nuclear localization has also been noted (Rayala et al., 2006). So far, it is unclear if different localizations are due to the type of cells investigated, experimental conditions, or possible modified variants of KIBRA.


The role of the KIBRA and APOE genes in developing spatial abilities in humans

In the contemporary high-tech society, spatial abilities predict individual life and professional success, especially in the STEM (Science, Technology, Engineering, and Mathematics) disciplines. According to neurobiological hypotheses, individual differences in cognitive abilities may be attributed to the functioning of genes involved in the regulation of neurogenesis and synaptic plasticity. In addition, genome-wide association studies identified rs17070145 located in the KIBRA gene, which was associated with individual differences in episodic memory. Considering a significant role of genetic and environmental components in cognitive functioning, the present study aimed to estimate the main effect of NGF (rs6330), NRXN1 (rs1045881, rs4971648), KIBRA (rs17070145), NRG1 (rs6994992), BDNF (rs6265), GRIN2B (rs3764030), APOE (rs7412, rs429358), and SNAP25 (rs363050) gene polymorphisms and to assess the effect of gene-environment interactions on individual differences in spatial ability in individuals without cognitive decline aged 18-25 years (N = 1011, 80 % women). Spatial abilities were measured using a battery of cognitive tests including the assessment of "3D shape rotation" (mental rotation). Multiple regression analysis, which was carried out in the total sample controlling for sex, ethnicity and the presence of the "risk" APOE ε4 allele, demonstrated the association of the rs17070145 Т-allele in the KIBRA gene with enhanced spatial ability (β = 1.32; pFDR = 0.037) compared to carriers of the rs17070145 CC-genotype. The analysis of gene-environment interactions revealed that nicotine smoking (β = 3.74; p = 0.010) and urban/rural residency in childhood (β = -6.94; p = 0.0002) modulated the association of KIBRA rs17070145 and АРОЕ (rs7412, rs429358) gene variants with individual differences in mental rotation, respectively. The data obtained confirm the effect of the KIBRA rs17070145 Т-allele on improved cognitive functioning and for the first time evidence the association of the mentioned genetic variant with spatial abilities in humans. A "protective" effect of the APOE ε2 allele on enhanced cognitive functioning is observed only under certain conditions related to childhood rearing.

Keywords: APOE; KIBRA; cognitive abilities; gene-environment interactions; linear regression; mental rotation.

 

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Next, we will look at the Klotho variant known as "KL-VS":

Sample Patient:

Klotho


Testing for Interactions Between APOE and Klotho Genotypes on Cognitive, Dementia, and Brain Imaging Metrics in UK Biobank​

Recent research suggests genetic variation in the Klotho locus may modify the association between APOE ɛ4 and cognitive impairment. We tested for associations and interactions between these genotypes versus risk of dementia, cognitive abilities, and brain structure in older UK Biobank participants. Klotho status was indexed with rs9536314 heterozygosity (versus not), in unrelated people with versus without APOE ɛ4 genotype, corrected for various confounders. APOE ɛ4 associated with increased risk of dementia, worse cognitive abilities, and brain structure. Klotho was associated with better reasoning. There were no interactions; potentially suggesting an age- and pathology-dependent Klotho effect.

 
No IQ for your face
 
big truth. sadly forum doesn't discuss high IQ privilege enough. IQ is just like looks mostly an immutable genetic trait. We need tax those fuckers :feelsree::feelsree::feelsree:
 

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