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Improvement of sleep quality is frequently correlated with an improvement in negative symptoms.Social isolation and or a lack of social constraint are routinely suggested as the cause of the sleep disruption in schizophrenia.Several of these genes are linked to sleep andor circadian regulation.For example, variants of disruptedinschizophrenia as well as to the homeostatic regulation of sleep in animal models.A polymorphism in cyclic AMP has been associated with sleepiness in one cohort study and with schizophrenia in another study. Furthermore, the TC single nucleotide polymorphism of the human CLOCK gene has been linked to abnormalities in dopamine regulation and to schizophrenia.Synaptosomalassociated protein protein that is essential for normal synaptic vesicle release from presynaptic nerve terminals and has been shown to play an important part in lightsignalling to the circadian system.Anxiety, panic, obsessivecompulsive disorder and posttraumatic stress disorder.Cause and effect, however, can be difficult to untangle for example, insomnia predisposes individuals to anxiety, which precipitates sleep disruption and this disruption then increases the likelihood of panic.Conversely, clinical research has shown that sleep Diethylstilbestrol problems may actually precede conditions such as anxiety and depression. In contrast to MDD, patients with PTSD and obsessivecompulsive disorder frequently show hypervigilance and problems in falling asleep.As a result, the diagnostic discrimination between anxiety disorder and delayed sleep phase syndrome has been linked in recent studies to anxiety and to sleep.For example, rodent studies have shown that nPS suppresses anxiety and appetite, induces wakefulness and hyperactivity, and plays a substantial part in the amelioration of conditioned fear. A specific polymorphism in the nPSR of men but not of women results in a gainoffunction of the receptor by increasing its sensitivity approximately tenfold.The less active isoform of the nPSR occurs less frequently in male patients with panic disorder and this suggests that nPS may have a potential protective function in panic disorders.In some neurodegenerative diseases the treatment of sleep abnormalities may even slow the progression of physical and mental decline.Below, we consider several neurodegenerative diseases that are commonly associated with sleep circadian rhythm disruption as well as those in which sleep stabilization has been shown to be beneficial.The general neurodegenerative process in AD undoubtedly alters many aspects of sleep and circadian control and certain changes have been suggested as markers of disease progression.In addition, degeneration of cholinergic neurons in the basal forebrain is one of the first biochemical changes that is noted in patients with AD.Activation of the cerebral cortex during REM sleep is dependent on the basal forebrains cholinergic innervations to the cerebral cortex.A disruption in this circuit is the Angelic Acid likely cause of REM sleep disruption in AD patients.This leads to the observed diminution of SWS and the increased nREM stage sleep.In addition, K complexes and sleep spindles, which are specific features of nREM stage sleep, are poorly formed, are of low amplitude, have a shorter duration and are less numerous.A link between sleep spindle number and verbal memory consolidation during sleep has been proposed in healthy subjects.Patients with AD also have a high prevalence of daytime sleeping and this can disrupt the homeostatic drivers for sleep.

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