In a two-way relationship, the sleep/wake cycle regulates amyloid-β levels and amyloid-β accumulation then disrupts sleep. A quantitative three-way model now suggests that amyloid-β impairs memory via its effect on sleep.
Mander and colleagues report that β-amyloid burden in medial prefrontal cortex correlates with severity of impairment in non-rapid eye movement slow wave activity (NREM SWA). This was further associated with impaired overnight memory consolidation and impoverished hippocampal-neocortical memory transformation.
Structural equation models revealed that the association between β-amyloid pathology and impaired hippocampus-dependent memory consolidation was not direct, but instead statistically depended on the intermediary factor of diminished NREM SWA. By linking β-amyloid pathology with impaired NREM SWA, the authors implicate sleep disruption as a pathway through which β-amyloid pathology may contribute to hippocampus-dependent cognitive decline in the elderly.
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Mander BA, Marks SM, Vogel JW, Rao V, Lu B, Saletin JM, Ancoli-Israel S, Jagust WJ, Walker MP: β-amyloid disrupts human NREM slow waves and related hippocampus-dependent memory consolidation. Nature Neuroscience 18: 1051–1057 (2015); doi:10.1038/nn.4035.
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http://www.ncbi.nlm.nih.gov/pubmed/26030850