Calcium signaling was found to be a central abnormality in schizophrenia neurons. Targeting calcium signaling in neurons could be a potential new way to treat the 16p11.2 duplication variation of schizophrenia.
Postmortem brains of those with schizophrenia have fewer genes associated with 12-hour activity cycles in the dorsolateral prefrontal cortex. Mitochondrial-related genes in the dlPFC did maintain a 12-hour rhythm, but their activity did not peak at normal times.
Investigating four pre-existing, publically available psychological and neurological data sets, researchers identify a network of brain areas that underlie psychiatric disorders including depression, anxiety, bipolar disorder, and schizophrenia.
By inhibiting NMDA receptors, ketamine increases noise to gamma frequencies in one layer of the thalamic nucleus and one lay of the somatosensory cortex. Findings suggest psychosis may be triggered by an increase in background noise impairing thalamocortical neurons which may be caused by a malfunction in NMDA receptors affecting the balance of inhibition and excitation in the brain.
Researchers identified 20 drug candidates that reduce C4 immune protein secretion from astrocytes. The discovery could pave the way to treating schizophrenia and other disorders associated with C4 dysregulation in astrocytes.
1% of patients registered in a health initiative carry at least one rare gene variant linked to an increased risk of a neuropsychiatric disorder such as schizophrenia or bipolar disorder. One third of those with a variant had been diagnosed with a mental health disorder.
People with schizophrenia have significantly higher rates of tandem repeats in their genome, up to 7% more than in people without the mental health disorder. The genes were primarily found in genes crucial to brain function.