-
Towards personalised neuromodulation in mental health: A non-invasive avenue of network research into dynamic brain circuits and their dysfunction
Prof. Marcus KaiserDone
-
From one-size-fits-all psychiatry to stratified psychiatry: Brain markers and heart-brain-coupling
Martijn Arns, PhDDone
-
Do I want to know? Artificial intelligence as a predictive tool in the diagnosis and treatment of cognitive impairment. Development of EEG-based functional network analyses
Prof. Ira Haraldsen, MDDone
-
Phase-amplitude coupling in EEG as a Parkinsonian biomarker
Prof. Thomas R. KnöscheDone
-
Clinical brain-computer interfaces: Challenges and new applications
Prof. Surjo Soekadar, MDDone
-
Neural markers of motor cognition: What do we know and what’s next?
Claudia Gianelli, PhDDone
-
Real brains in virtual worlds
Prof. Klaus GramannDone
-
Principles and challenges of fMRI-based ‘brain reading’
Prof. John-Dylan HaynesDone
-
Own data, not hardware
Cecilia Mazzetti, PhDDone
-
Schizophrenia: A temporal disorder?
Dr. Annemarie WolffDone
Professor Sophie Molholm is a Cognitive Neuroscientist at the Albert Einstein College of Medicine, with appointments
in the departments of Pediatrics, Neuroscience and Psychiatry and Behavioral Sciences. She uses multimodal brain imaging,
psychophysics, and standardized cognitive and clinical assessments to probe the brain processes underlying perception and
cognition in neurodevelopmental and neuropsychiatric conditions such as autism and schizophrenia as well as rare genetic disorders
including 22q11.2 deletion syndrome and Rett syndrome. Her research is supported by federal and foundation grants. In addition to
running her lab, she serves as Co-Director of the NIH funded Rose F. Kennedy Intellectual and Developmental Research Center, and
an NIH supported training grant for postdoctoral fellows engaged in research on intellectual and developmental disabilities.
22q11.2 Deletion Syndrome (22q11.2DS) is a multisystemic disorder characterized by a wide range of clinical features,
ranging from life-threatening to less severe conditions. One-third of individuals with the deletion live with mild to moderate intellectual
disability; approximately 60% meet criteria for at least one psychiatric condition. 22q11.2DS has become an important model for
several medical, developmental, and psychiatric disorders. We have been particularly interested in understanding the risk for psychosis
in this population: Approximately 30% of the individuals with the deletion go on to develop schizophrenia. The characterization of
cognitive and neural differences between those individuals who develop schizophrenia and those who do not, despite being at
genetic risk, holds important promise in what pertains to the clarification of paths to disease and to the development of tools for early
identification and intervention.
Here I will discuss our electrophysiological (EEG) findings as potential markers for 22q11.2DS and the associated risk for psychosis,
focusing on evidence from auditory processing (auditory-evoked potentials and auditory adaptation), visual processing (visual-evoked
potentials and visual adaptation), and inhibition and error monitoring. Altogether these data suggest basic mechanistic and disease
process effects on neural processing in 22q11.2DS that are present in both early sensory and later cognitive processing, with possible
implications for phenotype and relevance as markers for psychosis and risk for schizophrenia.