The role of the sleep K‐complex on the conversion from mild cognitive impairment to Alzheimer's disease.

Summary: The present literature points to an alteration of the human K‐complex during non‐rapid eye movement sleep in Alzheimer's disease. Nevertheless, the few findings on the K‐complex changes in mild cognitive impairment and their possible predictive role on the Alzheimer's disease conversion show mixed findings, lack of replication, and a main interest for the frontal region. The aim of the present study was to assess K‐complex measures in amnesic mild cognitive impairment subsequently converted in Alzheimer's disease over different cortical regions, comparing them with healthy controls and stable amnesic mild cognitive impairment. We assessed baseline K‐complex density, amplitude, area under the curve and overnight changes in frontal, central and parietal midline derivations of 12 amnesic mild cognitive impairment subsequently converted in Alzheimer's disease, 12 stable amnesic mild cognitive impairment and 12 healthy controls. We also assessed delta electroencephalogram power, to determine if K‐complex alterations in amnesic mild cognitive impairment occur with modification of the electroencephalogram power in the frequency range of the slow‐wave activity. We found a reduced parietal K‐complex density in amnesic mild cognitive impairment subsequently converted in Alzheimer's disease compared with stable amnesic mild cognitive impairment and healthy controls, without changes in K‐complex morphology and overnight modulation. Both amnesic mild cognitive impairment groups showed decreased slow‐wave sleep percentage compared with healthy controls. No differences between groups were observed in slow‐wave activity power. Our findings suggest that K‐complex alterations in mild cognitive impairment may be observed earlier in parietal regions, likely mirroring the topographical progression of Alzheimer's disease‐related brain pathology, and express a frontal predominance only in a full‐blown phase of Alzheimer's disease. Consistently with previous results, such K‐complex modification occurs in the absence of significant electroencephalogram power changes in the slow oscillations range. [ABSTRACT FROM AUTHOR]