Verging On Insanity: A genetic analysis of schizophrenia susceptibility in the hominoids

Research output: Contribution to conferenceAbstractpeer-review

Standard Standard

Verging On Insanity: A genetic analysis of schizophrenia susceptibility in the hominoids. / Ronan, Ella; Shaw, Vivien; Winder, Isabelle C.
2020. Abstract from PSGB Spring Meeting 2020, Liverpool, United Kingdom.

Research output: Contribution to conferenceAbstractpeer-review

HarvardHarvard

Ronan, E, Shaw, V & Winder, IC 2020, 'Verging On Insanity: A genetic analysis of schizophrenia susceptibility in the hominoids', PSGB Spring Meeting 2020, Liverpool, United Kingdom, 23/04/20 - 24/04/20.

APA

Ronan, E., Shaw, V., & Winder, I. C. (2020). Verging On Insanity: A genetic analysis of schizophrenia susceptibility in the hominoids. Abstract from PSGB Spring Meeting 2020, Liverpool, United Kingdom.

CBE

Ronan E, Shaw V, Winder IC. 2020. Verging On Insanity: A genetic analysis of schizophrenia susceptibility in the hominoids. Abstract from PSGB Spring Meeting 2020, Liverpool, United Kingdom.

MLA

Ronan, Ella, Vivien Shaw, and Isabelle C. Winder Verging On Insanity: A genetic analysis of schizophrenia susceptibility in the hominoids. PSGB Spring Meeting 2020, 23 Apr 2020, Liverpool, United Kingdom, Abstract, 2020.

VancouverVancouver

Ronan E, Shaw V, Winder IC. Verging On Insanity: A genetic analysis of schizophrenia susceptibility in the hominoids. 2020. Abstract from PSGB Spring Meeting 2020, Liverpool, United Kingdom.

Author

Ronan, Ella ; Shaw, Vivien ; Winder, Isabelle C. / Verging On Insanity: A genetic analysis of schizophrenia susceptibility in the hominoids. Abstract from PSGB Spring Meeting 2020, Liverpool, United Kingdom.

RIS

TY - CONF

T1 - Verging On Insanity: A genetic analysis of schizophrenia susceptibility in the hominoids

AU - Ronan, Ella

AU - Shaw, Vivien

AU - Winder, Isabelle C.

N1 - Poster presentation cancelled due to coronavirus; abstracts published in Primate Eye instead.

PY - 2020/4

Y1 - 2020/4

N2 - Schizophrenia, and the functional psychoses in general, are usually described as ‘human only’ afflictions. Lifetime prevalence rates of functional psychosis remain constant at 1-3%, while mental disorders account for 7.4% of the global disease burden. As our understanding of the severity and impact of mental disorders advances, more and more research is being undertaken to determine genetic causes of psychosis, albeit with little reference to evolutionary history. The rise in popularity of Genome Wide Association Studies (GWAS) has led to an increase in the rate of discovery of candidate genes linked to the onset and development of schizophrenic symptoms. Relatively little research has been done, however, on whether these same psychosis-associated genes can be found in other species. The African hominids in particular are the closest living relatives of Homo sapiens yet there is minimal literature examining their genomes for evidence of schizophrenia susceptibility alleles including DRD2, DISC1, DAOA, CACNA1C, ERBB4, NRG1, SRR, BDNF and FOXP2 (all of which are thought to be linked to human schizophrenia). In this study, we use MEGA-X to explore the published genomes of all species of African hominid, plus orangutans, gibbons and Old World monkeys, to see whether these genes are found in our close cousins and, if so, how different their alleles are from our own. One representative genome from each non-human primate group is then used along with sequences for the extinct Homo neanderthalensis and Denisovans to explore variation within our genus. Our findings provide an evolutionary context in which to re-consider the origins of functional psychosis. Furthermore, if we can find susceptibility genes in living non-human apes, we will have to re-evaluate the potential impact of psychoses on captive and wild hominoids, and re-consider our assumption that schizophrenia is fundamentally linked to being human.

AB - Schizophrenia, and the functional psychoses in general, are usually described as ‘human only’ afflictions. Lifetime prevalence rates of functional psychosis remain constant at 1-3%, while mental disorders account for 7.4% of the global disease burden. As our understanding of the severity and impact of mental disorders advances, more and more research is being undertaken to determine genetic causes of psychosis, albeit with little reference to evolutionary history. The rise in popularity of Genome Wide Association Studies (GWAS) has led to an increase in the rate of discovery of candidate genes linked to the onset and development of schizophrenic symptoms. Relatively little research has been done, however, on whether these same psychosis-associated genes can be found in other species. The African hominids in particular are the closest living relatives of Homo sapiens yet there is minimal literature examining their genomes for evidence of schizophrenia susceptibility alleles including DRD2, DISC1, DAOA, CACNA1C, ERBB4, NRG1, SRR, BDNF and FOXP2 (all of which are thought to be linked to human schizophrenia). In this study, we use MEGA-X to explore the published genomes of all species of African hominid, plus orangutans, gibbons and Old World monkeys, to see whether these genes are found in our close cousins and, if so, how different their alleles are from our own. One representative genome from each non-human primate group is then used along with sequences for the extinct Homo neanderthalensis and Denisovans to explore variation within our genus. Our findings provide an evolutionary context in which to re-consider the origins of functional psychosis. Furthermore, if we can find susceptibility genes in living non-human apes, we will have to re-evaluate the potential impact of psychoses on captive and wild hominoids, and re-consider our assumption that schizophrenia is fundamentally linked to being human.

M3 - Abstract

T2 - PSGB Spring Meeting 2020

Y2 - 23 April 2020 through 24 April 2020

ER -