Multiple non-redundant features of non-rapid eye movement sleep are altered in schizophrenia and largely independent of waking electrophysiological abnormalities, supporting the promise of neuropsychiatric disease biomarkers based on a precise dissection of the sleep.
An improved conditional gene-based association analysis framework guided by multiple variant-gene mapping strategies was built and evaluated based on its performance in predicting the potential susceptibility isoforms, genes, and tissues of schizophrenia.
Tineke Grent-'t-Jong, Joachim Gross ... Peter J Uhlhaas
Resting-state MEG-activity and MRS-GABA/Glx measurements reveal that there is a significant shift in excitability during the course of schizophrenia, involving hyperexcitability during the onset and a reduction at chronic stages.
DNA methylation data can be harnessed to provide insights into molecular and phenotypic differences associated with the spectrum of psychosis diagnoses.
Cortical network model suggests a mechanism explaining the link between NMDAR synaptic and spike synchrony deficits observed in a pharmacological monkey model of prefrontal network failure in schizophrenia.
A genetic program controlling brain genes across the lifespan specifies a calendar of changes in cells, synapses and behavioural genes thereby timing the onset of mental illnesses which arise in young adults.
The conditional reduction of glutaminase in mouse dopamine neurons selectively attenuates glutamate cotransmission at phasic frequencies, revealing the role of dopamine neuron glutamate cotransmission in the attribution of motivational salience.
In a mouse model of psychiatric illness, the neuronal network of the medial prefrontal cortex is characterized by reduced activity levels of interneurons, impaired gamma oscillations, and altered activation of cell assemblies.
Liquid biopsy methods utilizing brain-specific cell-free DNA methylation markers can detect brain cell death and potentially assist early detection and monitoring of schizophrenia.
Genetic rescue experiments reveal that γ-secretase enzymes containing Aph1b subunits control signalling by type III neuregulin 1, with implications for schizophrenia.