Cognitive impairment associated with neurodevelopmental disorders constitutes a substantial burden for affected individuals. With no effective treatment options at hand, resolving the cellular and neuronal network alterations that impair cognition is crucially important to lay the foundation for therapeutic interventions. Diverse etiologies are responsible for cognitive dysfunction, ranging from chromosomal anomalies to multifactorial environmental impacts on the basis of individual polygenic risk. In this symposium, we will discuss recent advances in our understanding of the genetic, cellular and network mechanisms responsible for altered cognition in neurodevelopmental disorders. We will contrast findings from different disease models with the goal to identify potential common motifs of network defects promoting cognitive impairment.

In the first part of the symposium, we will discuss the pathogenesis of cognitive defects in Down syndrome. Down syndrome arises by triplication of human chromosome 21, resulting in extra copies of about 300 genes. Affected patients suffer from intellectual disability and memory defects. To resolve how trisomy 21 causes cognitive impairment, it is vital to understand how triplication affects the functional properties of neuronal circuits. We will start the symposium with a talk by Elizabeth Fisher focusing on genetic mouse models of Down syndrome. Jan Schulz will then go on to present recent work on excitation/inhibition imbalance in Down syndrome.

In the second part of the symposium, we will discuss circuit malfunctions underlying cognitive deficits in psychiatric disorders, which emerge due to a complex interplay between environmental factors and genetic predisposition. In the third talk, Torfi Sigurdsson will examine cortical network alterations in a genetic mouse model of schizophrenia. Lucille Alonso (young investigator) will contribute recent results on a rat model of inducible serotonin depletion to study cognition defects. Finally, Ileana Hanganu-Opatz will uncover the mechanisms of developmental dysfunction underlying abnormal communications and cognitive disabilities in mice mimicking the etiology of schizophrenia.

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