Slow wave sleep deficits as a trait marker in patients with schizophrenia

Sarkar, Sukanto; Katshu, Mohammad Zia Ul Haq; Nizamie, S. Haque; Praharaj, Samir Kumar

doi:10.1016/j.schres.2010.08.013

Cited by 51 publications

(42 citation statements)

References 48 publications

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“…An examination of the heritability of sleep problems in SZ also points to familial factors. The PSG data of SZ nd their first degree relatives showed abnormal SWS a duration that was different from healthy controls [56]. These findings confirmed results of an early study of sleep abnormalities in relatives of SZ, that showed increased awaking after sleep onset (p = 0.06), reductions in SWS, decreased REM%, and decreased REM counts [57].…”

Section: Neurobiological Genetic and Environmental Factorssupporting

confidence: 79%

Sleep dysfunctions in schizophrenia: A practical review

Waters¹,

Manoach²

2012

OJPsych

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Section: Neurobiological Genetic and Environmental Factorssupporting

confidence: 79%

Sleep dysfunctions in schizophrenia: A practical review

Waters¹,

Manoach²

2012

OJPsych

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“…A number of studies confirm reductions in NREM, slow-wave sleep (SWS or N3) that correlate with measures of cognitive disorganization, impaired attention and disrupted declarative and procedural memory, hence impaired SWS is consistently linked to cognitive symptoms (Göder et al., 2006; Yang and Winkelman, 2006; Sarkar et al., 2010). Conversely, schizophrenic patients with mild cognitive symptoms do not show robust SWS deficits (Ferrarelli et al., 2010).…”

Section: Discussionmentioning

confidence: 99%

Decoupling of Sleep-Dependent Cortical and Hippocampal Interactions in a Neurodevelopmental Model of Schizophrenia

Phillips

Bartsch

McCarthy

et al. 2012

Neuron

118

123

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SummaryRhythmic neural network activity patterns are defining features of sleep, but interdependencies between limbic and cortical oscillations at different frequencies and their functional roles have not been fully resolved. This is particularly important given evidence linking abnormal sleep architecture and memory consolidation in psychiatric diseases. Using EEG, local field potential (LFP), and unit recordings in rats, we show that anteroposterior propagation of neocortical slow-waves coordinates timing of hippocampal ripples and prefrontal cortical spindles during NREM sleep. This coordination is selectively disrupted in a rat neurodevelopmental model of schizophrenia: fragmented NREM sleep and impaired slow-wave propagation in the model culminate in deficient ripple-spindle coordination and disrupted spike timing, potentially as a consequence of interneuronal abnormalities reflected by reduced parvalbumin expression. These data further define the interrelationships among slow-wave, spindle, and ripple events, indicating that sleep disturbances may be associated with state-dependent decoupling of hippocampal and cortical circuits in psychiatric diseases.

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“…In fact, administration of MPTP directly to the substantia nigra results in a decrease in REM sleep and a decrease in sleep latency (Lima et al, 2007). Further, both PD and schizophrenia are associated with sleep disorders although PD is related to a lack of dopamine and schizophrenia is related to an increase (Sarkar et al, 2010). It is possible that destruction of dopaminergic signaling in PD causes a breakdown in the control of wakefulness leading to increased excessive daytime sleepiness.…”

Section: Parkinson’s Diseasementioning

confidence: 99%

Sleep Disturbances in Alzheimer’s and Parkinson’s Diseases

Rothman

Mattson

2012

Neuromol Med

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Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the two most common neurodegenerative disorders, and exact a burden on our society greater than cardiovascular disease and cancer combined. While cognitive and motor symptoms are used to define AD and PD, respectively, patients with both disorders exhibit sleep disturbances including insomnia, hypersomnia and excessive daytime napping. The molecular basis of perturbed sleep in AD and PD may involve damage to hypothalamic and brainstem nuclei that control sleep – wake cycles. Perturbations in neurotransmitter and hormone signaling (e.g., serotonin, norepinephrine and melatonin) and the neurotrophic factor BDNF likely contribute to the disease process. Abnormal accumulations of neurotoxic forms of amyloid β-peptide, tau and α-synuclein occur in brain regions involved in the regulation of sleep in AD and PD patients, and are sufficient to cause sleep disturbances in animal models of these neurodegenerative disorders. Disturbed regulation of sleep often occurs early in the course of AD and PD, and may contribute to the cognitive and motor symptoms. Treatments that target signaling pathways that control sleep have been shown to retard the disease process in animal models of AD and PD, suggesting a potential for such interventions in humans at risk for, or in the early stages of these disorders.

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Slow wave sleep deficits as a trait marker in patients with schizophrenia

Cited by 51 publications

References 48 publications

Sleep dysfunctions in schizophrenia: A practical review

Sleep dysfunctions in schizophrenia: A practical review

Decoupling of Sleep-Dependent Cortical and Hippocampal Interactions in a Neurodevelopmental Model of Schizophrenia

Sleep Disturbances in Alzheimer’s and Parkinson’s Diseases

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