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X-WR-CALDESC:Events for Center for Behavior, Evolution, and Culture
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DTSTART;TZID=America/Los_Angeles:20121119T000000
DTEND;TZID=America/Los_Angeles:20121119T000000
DTSTAMP:20201013T004813Z
CREATED:20200922T215354Z
LAST-MODIFIED:20201013T004813Z
UID:4216-1353283200-1353283200@bec.ucla.edu
SUMMARY:Christina Palmer - Maternal-Fetal Genotype Incompatibility as a Risk Factor for Schizophrenia
DESCRIPTION:Christina Palmer: The University of California\, Los AngelesPrenatal/obstetric complications are implicated in schizophrenia susceptibility. Some complications may arise from maternal-fetal genotype incompatibility\, a term used to describe maternal-fetal genotype combinations that produce an adverse prenatal environment. As will be described\, maternal-fetal genotype incompatibility can occur when maternal and fetal genotypes differ from one another\, or when maternal and fetal genotypes are too similar to each other. Incompatibility genes for each of these scenarios have been implicated as risk factors for schizophrenia and a review of maternal-fetal genotype incompatibility studies suggests that schizophrenia susceptibility is increased by maternal-fetal genotype combinations at the RHD\, ABO\, and HLA-B loci. Maternal-fetal genotype combinations at these loci are hypothesized to have an effect on the maternal immune system during pregnancy\, which can affect fetal neurodevelopment and increase schizophrenia susceptibility. During this presentation\, data will be synthesized and the hypothesized biological role of these incompatibility genes in the etiology of schizophrenia will be described.
URL:https://bec.ucla.edu/event/christina-palmer-maternal-fetal-genotype-incompatibility-as-a-risk-factor-for-schizophrenia/
CATEGORIES:Past Presentation,Presentation
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DTSTART;TZID=America/Los_Angeles:20121126T000000
DTEND;TZID=America/Los_Angeles:20121126T000000
DTSTAMP:20201013T004813Z
CREATED:20200922T215354Z
LAST-MODIFIED:20201013T004813Z
UID:4217-1353888000-1353888000@bec.ucla.edu
SUMMARY:Georg Striedter - What's Special About Human Brains?
DESCRIPTION:Georg Striedter: The University of California\, Irvine. Human brains are much larger than one would expect for primates of our body size.  They also feature more neurons and a proportionately larger neocortex.  Prefrontal cortex\, in particular\, is significantly larger in humans than in other species. Although these features make the human brain unique\, most of them are in line with allometric expectations\, meaning that they can be predicted from the large size of our brains. Thus\, human brains are fairly typical primate brains; they just became unusually large.  Nonetheless\, there are good reasons to believe that the evolutionary expansion of the human brain\, especially of prefrontal cortex\, caused evolutionary changes in neural connectivity and function.  Dr. Striedter will review some of the evidence supporting this idea and place it in the larger context of brain and behavioral evolution.
URL:https://bec.ucla.edu/event/georg-striedter-whats-special-about-human-brains/
CATEGORIES:Past Presentation,Presentation
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