Sleep-dependent memory consolidation in healthy aging and mild cognitive impairment

Abstract

Sleep quality and architecture as well as sleep’s homeostatic and circadiancontrols change with healthy aging. Changes include reductions in slow-wavesleep’s (SWS) percent and spectral power in the sleep electroencephalogram (EEG),number and amplitude of sleep spindles, rapid eye movement (REM) density and theamplitude of circadian rhythms, as well as a phase advance (moved earlier in time)of the brain’s circadian clock. With mild cognitive impairment (MCI) there arefurther reductions of sleep quality, SWS, spindles, and percent REM, all of whichfurther diminish, along with a profound disruption of circadian rhythmicity, with theconversion to Alzheimer’s disease (AD). Sleep disorders may represent risk factorsfor dementias (e.g., REM Behavior Disorder presages Parkinson’s disease) andsleep disorders are themselves extremely prevalent in neurodegenerative diseases.Working memory, formation of new episodic memories, and processing speed alldecline with healthy aging whereas semantic, recognition, and emotional declarativememory are spared. In MCI, episodic and working memory further declinealong with declines in semantic memory. In young adults, sleep-dependent memoryconsolidation (SDC) is widely observed for both declarative and proceduralmemory tasks. However, with healthy aging, although SDC for declarative memoryis preserved, certain procedural tasks, such as motor-sequence learning, do not showSDC. In younger adults, fragmentation of sleep can reduce SDC, and a normative