BEGIN:VCALENDAR
VERSION:2.0
PRODID:-//SFARI - ECPv6.6.3//NONSGML v1.0//EN
CALSCALE:GREGORIAN
METHOD:PUBLISH
X-ORIGINAL-URL:https://www.sfari.org
X-WR-CALDESC:Events for SFARI
REFRESH-INTERVAL;VALUE=DURATION:PT1H
X-Robots-Tag:noindex
X-PUBLISHED-TTL:PT1H
BEGIN:VTIMEZONE
TZID:UTC
BEGIN:STANDARD
TZOFFSETFROM:+0000
TZOFFSETTO:+0000
TZNAME:UTC
DTSTART:20160101T000000
END:STANDARD
END:VTIMEZONE
BEGIN:VEVENT
DTSTART;TZID=UTC:20161102T170000
DTEND;TZID=UTC:20161102T181500
DTSTAMP:20260513T150835
CREATED:20161102T080000Z
LAST-MODIFIED:20180216T201644Z
UID:2010-1478106000-1478110500@www.sfari.org
SUMMARY:How immune cells help wire the brain: Implications for autism and psychiatric illness
DESCRIPTION:  \nOn 2 November 2016\, Beth Stevens discussed recent work that implicates brain immune cells\, called microglia\, in sculpting of synaptic connections during development and their relevance to autism\, schizophrenia and other brain disorders. \nHer talk was part of the Simons Foundation Autism Research lecture series. \nAbout the Lecture\nRecent research has revealed a key role for microglia and a group of immune-related molecules\, called complement\, in normal developmental synaptic pruning\, a process required to establish precise brain wiring. Emerging evidence from Beth Stevens’ lab and others suggest aberrant regulation of this pruning pathway may contribute to synaptic and cognitive dysfunction in a host of brain disorders\, including schizophrenia. Studies also suggest that a person’s risk of schizophrenia is increased if he or she inherits specific variants in complement C4\, which plays a well-known role in the immune system but also helps sculpt developing synapses in the mouse visual system. \nTogether these findings may help explain known features of schizophrenia\, including reduced numbers of synapses in key cortical regions and an adolescent age of onset that corresponds with developmentally timed waves of synaptic pruning in these regions. Stevens discussed this and ongoing work to understand the mechanisms by which complement and microglia prune specific synapses in the brain. A deeper understanding of how these immune mechanisms mediate synaptic pruning may provide novel insight into how to protect synapses in autism and other brain disorders. \nAbout the speaker\nBeth Stevens is an assistant professor of neurology at Harvard Medical School and the F.M. Kirby Neurobiology Center at Boston Children’s Hospital and a member of the Broad Institute. Her laboratory seeks to understand how neuron-glia communication facilitates the formation\, elimination and plasticity of synapses during both healthy development and disease states. Stevens is a recipient of several young investigator awards\, including the Ellison Medical Foundation New Scholar in Aging; John Merck Scholar Program; Presidential Early Career Award for Scientists and Engineers; and a MacArthur Fellowship. \n  \n 
URL:https://www.sfari.org/event/how-immune-cells-help-wire-the-brain-implications-for-autism-and-psychiatric-illness/
LOCATION:Gerald D. Fischbach Auditorium\, 160 5th Avenue\, New York\, NY\, 10010\, United States
ATTACH;FMTTYPE=image/jpeg:https://sf-web-assets-prod.s3.amazonaws.com/wp-content/uploads/sites/2/2017/07/04170132/BethStevens250.jpg
END:VEVENT
END:VCALENDAR