DGPPN Kongressprogramm 2014 - page 50

BESONDERE VERANSTALTUNGEN 50
PLENARVORTRÄGE
mi, 26. 11. 2014 | 12.45 – 13.45 uhr | saal a6 / 7
E
U
D
Towards molecular insights into autism and
schizophrenia pathogenesis: Neurexins and company
Thomas C. Südhof, Stanford (USA)
Vorsitz:
Wolfgang Maier, Bonn
Peter Falkai, München
© Alena Soboleva
Neurexins and neuroligins are synaptic cell-adhesion molecules that are essential for sy-
napse formation and function. Mutations in neurexin and neuroligin genes and in genes
encoding proteins binding to neurexins or neuroligins have been implicated in autism and
schizophrenia. In fact, mutations of the neurexin-1 gene (NRXN1) may at present be the
only identified single gene mutation that has been repeatedly associated with schizophre-
nia, with more than 100 independent families. Neurexins are presynaptic cell-adhesion
molecules that are encoded by three extraordinarily large genes, each of which genera-
tes longer
α
- and shorter
β
-isoforms that are in turn diversified into multiple alternatively
spliced transcripts. Presynaptic neurexins bind to a series of ligands, including postsynaptic
cell-adhesion molecules of the neuroligin and the LRRTM families that are each encoded by
four genes. The various splice variants of neurexins and the various isoforms of neuroligins
and LRRTMs exhibit strikingly different functional activities, and contribute to determining
the properties and nature of synapses. Accumulating evidence demonstrates that neurexins
and neuroligins and their additional ligands perform central functions in the assembly and
function of neural circuits, but their precise roles and mechanisms of action are beginning
to emerge. Moreover, the potential mechanisms by which mutations in neurexins, neuro-
ligins, and LRRTMs may contribute to the pathogenesis of autism or schizophrenia are
only now being studied. In my talk, I will describe our recent studies on how neurexins
and their ligands (‘company’) shape synapse properties, and how mutations in these genes
may produce synapse dysfunction that may plausible account for autism and schizophrenia
pathogenesis.
mi, 26. 11. 2014 | 14.00 – 15.00 uhr | saal a6 / 7
E
U
D
The neurobiology of child abuse and neglect
Charles B. Nemeroff, Miami (USA)
Vorsitz:
Andreas Heinz, Berlin
Thomas E. Schläpfer, Bonn
1...,40,41,42,43,44,45,46,47,48,49 51,52,53,54,55,56,57,58,59,60,...
Powered by FlippingBook