Topic: psychiatric diseases

Sleep deficits are often prodromal to the onset of psychiatric diseases. Such disorders, for example schizophrenia, autism spectrum disorder or attention deficit hyperactivity disorder, are strongly linked to the 22q11.2 microdeletion (22qdel). Carriers of 22qdel exhibit reduced sleep spindle formation, which correlates to decreased memory performance and disease severity. Two neurological cell populations, the noradrenergic (NA) neurons in the locus coeruleus (LC) and the parvalbumin (PV)-positive cortical interneurons are involved in the regulation of sleep spindles. However, the interplay o

Deficits in reward processing are a characteristic symptomatic dimension of psychiatric diseases such as major depression, bipolar disorder and schizophrenia. These deficits have been linked to the dysfunction of the mesocorticolimbic dopamine transmission suggesting the existence of common underlying pathophysiological mechanisms. Numerous clinical studies have described a decrease in n-3 polyunsaturated fatty acids (PUFAs) in subpopulations of patients suffering from psychiatric disorders (Conklin et al., 2010; Messamore and McNamara, 2016). Moreover, preclinical results from our laboratory