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.
journal_name
Nat Neuroscijournal_title
Nature neuroscienceauthors
Mander BA,Marks SM,Vogel JW,Rao V,Lu B,Saletin JM,Ancoli-Israel S,Jagust WJ,Walker MPdoi
10.1038/nn.4035subject
Has Abstractpub_date
2015-07-01 00:00:00pages
1051-7issue
7eissn
1097-6256issn
1546-1726pii
nn.4035journal_volume
18pub_type
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