Abstract
Sleep disturbances and memory dysfunction are key characteristics across psychiatric disorders. Recent advances have revealed insight into the role of sleep in memory consolidation, pointing to key overlap between memory consolidation processes and structural and molecular abnormalities in psychiatric disorders. Ongoing research regarding the molecular mechanisms involved in memory consolidation has the potential to identify therapeutic targets for memory dysfunction in psychiatric disorders and aging. Recent evidence from our group and others points to extracellular matrix molecules, including chondroitin sulfate proteoglycans and their endogenous proteases, as molecules that may underlie synaptic dysfunction in psychiatric disorders and memory consolidation during sleep. These molecules may provide a therapeutic targets for decreasing strength of reward memories in addiction and traumatic memories in PTSD, as well as restoring deficits in memory consolidation in schizophrenia and aging. We review the evidence for sleep and memory consolidation dysfunction in psychiatric disorders and aging in the context of current evidence pointing to the involvement of extracellular matrix molecules in these processes.
Highlights
Sleep and circadian rhythm disturbances are emerging as shared features across psychiatric disorders and aging, and are strongly associated with memory consolidation and synaptic dysfunction
We review the current evidence for sleep and memory consolidation dysfunction in psychiatric disorders and aging, in the context of the potential extracellular matrix molecules as a key molecules in memory consolidation dysfunction
We recently reported broad alterations of Extracellular matrix molecules (ECM) molecule gene expression in subjects with SZ associated with cognitive deficits, impacting Chondroitin sulfate proteoglycans (CSPGs) core proteins, chondroitin sulfate synthesis pathways, and endogenous proteases across several cortical and subcortical brain regions (Pantazopoulos et al, 2020b)
Summary
Sleep and circadian rhythm disturbances are emerging as shared features across psychiatric disorders and aging, and are strongly associated with memory consolidation and synaptic dysfunction. This work demonstrates that sleep promotes dendritic spine formation of motor memory in selective branches of layer V motor cortex neurons (Yang et al, 2014), These studies support the hypothesis that sleep is involved in strengthening selective synapses formed during wakefulness for selective memories, and this occurs even in cortical areas where net synaptic downscaling during sleep has been reported (Maret et al, 2011; de Vivo et al, 2017) Such discrepancies have been proposed to arise from methodological differences, differences in sleep deprivation methods (Havekes and Aton, 2020). Several studies, including seminal work in the visual cortex and the amygdala, demonstrated that PNNs form during the end of critical periods
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