Possible link between Alzheimer's disease and disrupted sleep-dependent memory consolidation?
It would also be interesting to investigate possible disruptions in thalamic sleep spindle activity to see how this may further contribute to memory impairment in this population. I wrote about this possibility in my Sleep Medicine Review's paper a few years ago.
Here is Mander et al.'s abstract, which appears under the advanced online publication section of Nature Neuroscience:
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.
Reference:
Mander, B.,A., Marks, S.,M., Vogel, J.,W., Rao, ,Vikram, Lu, ,Brandon, Saletin, J.,M., . . . Walker, M.,P.Beta]-amyloid disrupts human NREM slow waves and related hippocampus-dependent memory consolidation.
Lu, W., & Göder, R. (2012). Does abnormal non-rapid eye movement sleep impair declarative memory consolidation? Sleep Medicine Reviews, 16 (4), 389-394 DOI: 10.1016/j.smrv.2011.08.001
