article i nfo Evidencesuggeststhatamyloid-beta (Aβ) depositions parallelsleep deficits inAlzheimer'sdisease (AD).Howev- er, it remains unknown whether impaired sleep and changes in plasma Aβ levels are related in amnestic mild cognitive impairment (aMCI) subjects, and whether both markers are further associated with cortical thinning in canonical AD regions. To jointly address this issue, we investigated relationships between changes in physio- logical sleep and plasma Aβ concentrations in 21 healthy old (HO) adults and 21 aMCI subjects, and further assessed whether these two factors were associated with cortical loss in each group. aMCI, but not HO subjects, showedsignificantrelationshipsbetween disruptedslow-wave sleep(SWS) and increasedplasmalevelsof Aβ42. Wealsofoundthatshortenedrapid-eyemovement(REM)sleepinaMCIcorrelatedwiththinningoftheposterior cingulate, precuneus, and postcentral gyrus; whereas higher levels of Aβ40 and Aβ42 accounted for grey matter (GM) loss of posterior cingulate and entorhinal cortex, respectively. These results support preliminary relation- ships between Aβ burden and altered sleep physiology observed in animal models of AD amyloidosis, and provide precise cortical correlates of these changes in older adults with aMCI. Taken together, these findings open new research avenues on the combined role of sleep, peripheral Aβ levels and cortical integrity in tracking the progression from normal aging to early neurodegeneration.
['Mayely P. Sanchez-Espinosa', 'Mercedes Atienza', 'Jose L. Cantero']
Sleep deficits in mild cognitive impairment are related to increased levels of plasma amyloid-β and cortical thinning.