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Nat Neurosci. 2015 Jul;18(7):1051-7. doi: 10.1038/nn.4035. Epub 2015 Jun 1.

β-amyloid disrupts human NREM slow waves and related hippocampus-dependent memory consolidation.

Author information

1
Sleep and Neuroimaging Laboratory, University of California, Berkeley, California, USA.
2
Helen Wills Neuroscience Institute, University of California, Berkeley, California, USA.
3
Division of Pulmonary and Critical Care Medicine, California Pacific Medical Center, San Francisco, California, USA.
4
Department of Psychiatry, University of California, San Diego, La Jolla, California, USA.
5
1] Helen Wills Neuroscience Institute, University of California, Berkeley, California, USA. [2] Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California, USA.
6
1] Sleep and Neuroimaging Laboratory, University of California, Berkeley, California, USA. [2] Helen Wills Neuroscience Institute, University of California, Berkeley, California, USA.

Abstract

Independent evidence associates β-amyloid pathology with both non-rapid eye movement (NREM) sleep disruption and memory impairment in older adults. However, whether the influence of β-amyloid pathology on hippocampus-dependent memory is, in part, driven by impairments of NREM slow wave activity (SWA) and associated overnight memory consolidation is unknown. Here we show that β-amyloid burden in medial prefrontal cortex (mPFC) correlates significantly with the severity of impairment in NREM SWA generation. Moreover, reduced NREM SWA generation was further associated with impaired overnight memory consolidation and impoverished hippocampal-neocortical memory transformation. Furthermore, structural equation models revealed that the association between mPFC 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, these data implicate sleep disruption as a mechanistic pathway through which β-amyloid pathology may contribute to hippocampus-dependent cognitive decline in the elderly.

PMID:
26030850
PMCID:
PMC4482795
DOI:
10.1038/nn.4035
[Indexed for MEDLINE]
Free PMC Article

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