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"Intellect Genetic aspects."
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Genes, Brains, and Human Potential
For countless generations people have been told that their potential as humans is limited and fundamentally unequal. The social order, they have been assured, is arranged by powers beyond their control. More recently the appeal has been to biology, specifically the genes, brain sciences, the concept of intelligence, and powerful new technologies. Reinforced through the authority of science and a growing belief in bio-determinism, the ordering of the many for the benefit of a few has become more entrenched. Yet scientists are now waking up to the influence of ideology on research and its interpretation. In Genes, Brains, and Human Potential, Ken Richardson illustrates how the ideology of human intelligence has infiltrated genetics, brain sciences, and psychology, flourishing in the vagueness of basic concepts, a shallow nature-versus-nurture debate, and the overhyped claims of reductionists. He shows how ideology, more than pure science, has come to dominate our institutions, especially education, encouraging fatalism about the development of human intelligence among individuals and societies. Genes, Brains, and Human Potential goes much further: building on work being done in molecular biology, epigenetics, dynamical systems, evolution theory, and complexity theory, it maps a fresh understanding of intelligence and the development of human potential. Concluding with an upbeat message for human possibilities, this synthesis of diverse perspectives will engender new conversations among students, researchers, and other interested readers.
eBook
The mismeasure of minds : debating race and intelligence between Brown and The bell curve
\"The 1954 Brown v. Board of Education decision required desegregation of America's schools, but it also set in motion an agonizing multi-decade debate over race, class, and IQ. In this innovative book, Michael E. Staub investigates neuropsychological studies published between Brown and the controversial 1994 book, The Bell Curve. In doing so, he illuminates how we came to view race and intelligence today\"-- Provided by publisher.
BOOK
Brain and race : a history of cerebral anthropology
For nearly two centuries, the racial significance of the human brain has absorbed a huge amount of scientific energy, despite the frequency of shortcomings and disappointing results. This book tries to show and explain the resilience of such a thorny issue.
eBook
Intelligence testing and minority students : foundations, performance factors, and assessment issues
Intelligence Testing and Minority Students offers the reader a fresh opportunity to re-learn and re-consider the implications of intelligence testing. Richard R. Valencia and Lisa A. Suzuki discuss the strengths and limitations of IQ testing relative to the factors which may contribute to biased results. They review the history of the adaptation and adoption of intelligence testing; evaluate the heredity-environment debate; discuss the specific performance factors which apply to IQ testing of those in minority ethnic groups. This practical book offers the practitioner a good sense of what can be done to make testing and education serve the needs of all students fairly and validly, whatever their background.
eBook
Mental retardation and developmental delay : genetic and epigenetic factors
Recent advances in neuroscience and genetics have greatly expanded our understanding of the brain and of the etiological factors involved in developmental delay and mental retardation. At the same time, the human genome project has yielded a wealth of information on DNA sequencing, regulation of gene expression, epigenetics, and functional aspects of the genome, which newly propels investigation into the pathogenesis of mental retardation. This book makes readily available current knowledge on the subject and applies it to clinical medicine, providing information essential to neurologists, geneticists, physicians and pediatricians as they search for the causes of mental handicap in their patients. Introductory chapters cover normal and abnormal brain structure, neurogenesis, neuronal proliferation, and signal transduction. Latter chapters delve into discussions of both the environmental factors that may lead to neurocognitive deficits and the cytogenetic, biochemical and molecular defects specifically associated with mental retardation. One chapter reviews gene involvement in non-syndromic mental retardation, autism, and language deficits, as well as multifactorial and genetically complex inheritance. The text concludes with a clinically practical discussion of carrier detection, presymptomatic diagnosis, and treatment of various genetic diseases through enzyme therapy, substrate deprivation, and the use of hemapoietic stem cells.
eBook
Using common genetic variation to examine phenotypic expression and risk prediction in 22q11.2 deletion syndrome
The 22q11.2 deletion syndrome (22q11DS) is associated with a 20–25% risk of schizophrenia. In a cohort of 962 individuals with 22q11DS, we examined the shared genetic basis between schizophrenia and schizophrenia-related early trajectory phenotypes: sub-threshold symptoms of psychosis, low baseline intellectual functioning and cognitive decline. We studied the association of these phenotypes with two polygenic scores, derived for schizophrenia and intelligence, and evaluated their use for individual risk prediction in 22q11DS. Polygenic scores were not only associated with schizophrenia and baseline intelligence quotient (IQ), respectively, but schizophrenia polygenic score was also significantly associated with cognitive (verbal IQ) decline and nominally associated with sub-threshold psychosis. Furthermore, in comparing the tail-end deciles of the schizophrenia and IQ polygenic score distributions, 33% versus 9% of individuals with 22q11DS had schizophrenia, and 63% versus 24% of individuals had intellectual disability. Collectively, these data show a shared genetic basis for schizophrenia and schizophrenia-related phenotypes and also highlight the future potential of polygenic scores for risk stratification among individuals with highly, but incompletely, penetrant genetic variants.
Polygenic risk scores are nearing a level of differentiation required for their clinical utility in risk prediction in populations with high-risk rare pathogenic genetic variants.
Journal Article
Rates, distribution and implications of postzygotic mosaic mutations in autism spectrum disorder
Survey of postzygotic mosaic mutations (PZMs) in 5,947 trios with autism spectrum disorders (ASD) discovers differences in mutational properties between germline mutations and PZMs. Spatiotemporal analyses of the PZMs also revealed the association of the amygdala with ASD and implicated risk genes, including recurrent potential gain-of-function mutations in
SMARCA4
.
We systematically analyzed postzygotic mutations (PZMs) in whole-exome sequences from the largest collection of trios (5,947) with autism spectrum disorder (ASD) available, including 282 unpublished trios, and performed resequencing using multiple independent technologies. We identified 7.5% of
de novo
mutations as PZMs, 83.3% of which were not described in previous studies. Damaging, nonsynonymous PZMs within critical exons of prenatally expressed genes were more common in ASD probands than controls (
P
< 1 × 10
−6
), and genes carrying these PZMs were enriched for expression in the amygdala (
P
= 5.4 × 10
−3
). Two genes (
KLF16
and
MSANTD2
) were significantly enriched for PZMs genome-wide, and other PZMs involved genes (
SCN2A
,
HNRNPU
and
SMARCA4
) whose mutation is known to cause ASD or other neurodevelopmental disorders. PZMs constitute a significant proportion of
de novo
mutations and contribute importantly to ASD risk.
Journal Article
De novo variants in neurodevelopmental disorders with epilepsy
Epilepsy is a frequent feature of neurodevelopmental disorders (NDDs), but little is known about genetic differences between NDDs with and without epilepsy. We analyzed de novo variants (DNVs) in 6,753 parent–offspring trios ascertained to have different NDDs. In the subset of 1,942 individuals with NDDs with epilepsy, we identified 33 genes with a significant excess of DNVs, of which
SNAP25
and
GABRB2
had previously only limited evidence of disease association. Joint analysis of all individuals with NDDs also implicated
CACNA1E
as a novel disease-associated gene. Comparing NDDs with and without epilepsy, we found missense DNVs, DNVs in specific genes, age of recruitment, and severity of intellectual disability to be associated with epilepsy. We further demonstrate the extent to which our results affect current genetic testing as well as treatment, emphasizing the benefit of accurate genetic diagnosis in NDDs with epilepsy.
Analysis of individuals with neurodevelopmental disorders (NDDs) with epilepsy identifies 33 genes with a significant excess of de novo variants. Comparison of rates of de novo variants between NDDs with or without epilepsy highlights differences between these phenotypic groups.
Journal Article
Meta-analysis of 2,104 trios provides support for 10 new genes for intellectual disability
The authors analyzed the exome sequences of 2,104 intellectual disability patients and their parents. They identified 10 novel candidate genes associated with specific clinical phenotypes.
To identify candidate genes for intellectual disability, we performed a meta-analysis on 2,637
de novo
mutations, identified from the exomes of 2,104 patient–parent trios. Statistical analyses identified 10 new candidate ID genes:
DLG4
,
PPM1D
,
RAC1
,
SMAD6
,
SON
,
SOX5
,
SYNCRIP
,
TCF20
,
TLK2
and
TRIP12
. In addition, we show that these genes are intolerant to nonsynonymous variation and that mutations in these genes are associated with specific clinical ID phenotypes.
Journal Article