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Books on the topic 'Human neurogenesis'

Author: Grafiati

Published: 16 November 2024

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1

Winter, Robin M. London dysmorphology database: &, London neurogenetics database. 2nd ed. Oxford: Oxford University Press, 1998.

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2

Winter, Robin M. London dysmorphology database. 2nd ed. Oxford: Oxford University Press, 1996.

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3

R, Hayden Michael, and Rubinsztein D. C, eds. Analysis of triplet repeat disorders. Oxford: Bios Scientific Publishers, 1998.

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4

Sutcliffe, Alastair. Congenital anomalies: Case studies and mechanisms. Rijeka, Croatia: InTech, 2012.

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5

D, Wells R., Warren Stephen T, and Sarmiento Marion, eds. Genetic instabilities and hereditary neurological diseases. San Diego, Calif: Academic Press, 1998.

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6

1946-, Oostra Ben A., ed. Trinucleotide diseases and instability. Berlin: Springer, 1998.

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7

Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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8

Cryan, John F., and Andreas Reif. Behavioral Neurogenetics. Springer, 2014.

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9

Cryan, John F., and Andreas Reif. Behavioral Neurogenetics. Springer, 2012.

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10

Cryan, John F., and Andreas Reif. Behavioral Neurogenetics. Springer London, Limited, 2012.

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11

Ebstein, Richard P., Songfa Zhong, Robin Chark, Poh San Lai, and Soo Hong Chew. Modeling the Genetics of Social Cognition in the Laboratory. Edited by Turhan Canli. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.017.

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This chapter examines recent advances in the genetics of social cognition, discussing evidence from twin studies that confirm the relevancy of genetic hard wiring in understanding many social phenotypes, with important implications for the social sciences and for genome-wide association studies (GWAS) that may identify specific genes contributing to a wide range of social phenotypes, genoeconomics, and individual and social decision making. Stressing the importance of phenotype definition and precise measurement as key to success in GWAS, the authors argue that laboratory-based behavioral economic paradigms using ethnically homogenous student populations generate the best prospects for successful GWAS. Also discussed are the neurochemical/neurogenetic architecture of behavioral economic games that measure individual and social decision making and the considerable progress made in unraveling the neurogenetics of human parenting and the beginning of a political attitudes neuroscience. The authors’ own GWAS is used to present a set of guidelines for future research directions.

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12

Jenner, Peter, Ronald J. Bradley, F. Clifford Rose, and Adron R. Harris. Neurobiology of Painting: International Review of Neurobiology. Elsevier Science & Technology Books, 2006.

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13

Hanaei, Sara, and Nima Rezaei. Human Brain and Spinal Cord Tumors : from Bench to Bedside. Volume 1: Neuroimmunology and Neurogenetics. Springer International Publishing AG, 2022.

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14

Human Brain and Spinal Cord Tumors : from Bench to Bedside. Volume 1: Neuroimmunology and Neurogenetics. Springer International Publishing AG, 2024.

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15

Buckholtz, Joshua W., and Andreas Meyer-Lindenberg. Genetic Perspectives on the Neurochemistry of Human Aggression and Violence. Edited by Turhan Canli. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.009.

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Violence is a devastating social phenomenon that is costly both to affected individuals and to society at large. Pathological aggression, especially reactive/impulsive aggression, is a cardinal symptom common to several psychiatric disorders—including antisocial personality disorder, borderline personality disorder, and psychopathy—that are associated with risk for violence. Thus, understanding the factors that predispose people to impulsive violence represents a crucial goal for psychology, neuroscience, and psychiatry. Although we are far from a full understanding of the etiopathophysiology of violence, impulsive aggression is heritable, suggesting that genetic mechanisms may be important for determining individual variation in susceptibility. This chapter synthesizes available preclinical and human data to propose a compelling neurogenetic mechanism for violence, specifically arguing that a genetically determined excess in serotonin signaling during a critical developmental period leads to dysregulation within a key corticolimbic circuit for emotional arousal and regulation, inhibitory control, and social cognition.

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16

Genetic Instabilities and Neurological Diseases, Second Edition, Second Edition. 2nd ed. Academic Press, 2006.

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17

Oostra, Ben A. Trinucleotide Diseases and Instability. Springer Berlin / Heidelberg, 2013.

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18

(Editor), Robert D. Wells, and Tetsuo Ashizawa (Editor), eds. Genetic Instabilities and Neurological Diseases, Second Edition, Second Edition. Academic Press, 2006.

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19

Oostra, Ben A. Trinucleotide Diseases and Instability. Springer London, Limited, 2013.

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20

Numan, Michael. Neurobiology of Social Behavior: Toward an Understanding of the Prosocial and Antisocial Brain. Elsevier Science & Technology Books, 2014.

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21

Numan, Michael. Neurobiology of Social Behavior: Toward an Understanding of the Prosocial and Antisocial Brain. Elsevier Science & Technology Books, 2014.

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22

(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.

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