Journal
ANNUAL REVIEW OF CLINICAL PSYCHOLOGY, VOL 15
Volume 15, Issue -, Pages 451-479Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev-clinpsy-050718-095754
Keywords
cognition; endophenotype; genetics; memory; schizophrenia; sleep; spindles
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Funding
- NIMH NIH HHS [R01 MH048832, R01 MH107579, K24 MH099421, R01 MH092638] Funding Source: Medline
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There is overwhelming evidence that sleep is crucial for memory consolidation. Patients with schizophrenia and their unaffected relatives have a specific deficit in sleep spindles, a defining oscillation of non-rapid eye movement (NREM) Stage 2 sleep that, in coordination with other NREM oscillations, mediate memory consolidation. In schizophrenia, the spindle deficit correlates with impaired sleep-dependent memory consolidation, positive symptoms, and abnormal thalamocortical connectivity. These relations point to dysfunction of the thalamic reticular nucleus (TRN), which generates spindles, gates the relay of sensory information to the cortex, and modulates thalamocortical communication. Genetic studies are beginning to provide clues to possible neurodevelopmental origins of TRN-mediated thalamocortical circuit dysfunction and to identify novel targets for treating the related memory deficits and symptoms. By forging empirical links in causal chains from risk genes to thalamocortical circuit dysfunction, spindle deficits, memory impairment, symptoms, and diagnosis, future research can advance our mechanistic understanding, treatment, and prevention of schizophrenia.
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