Table of Contents Author Guidelines Submit a Manuscript
International Journal of Alzheimer’s Disease
Volume 2011 (2011), Article ID 214580, 7 pages
Research Article

Direction of Information Flow in Alzheimer's Disease and MCI Patients

1AfaR, Department of Neuroscience, Fatebenefratelli Hospital, Isola Tiberina, 00186 Rome, Italy
2Department of Imaging, San Raffaele Cassino, 03043 Cassino, Italy
3Department of Biomedical Sciences, University of Foggia, 71100 Foggia, Italy

Received 14 December 2010; Accepted 13 February 2011

Academic Editor: Sara Määttä

Copyright © 2011 Fabrizio Vecchio and Claudio Babiloni. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Is directionality of electroencephalographic (EEG) synchronization abnormal in amnesic mild cognitive impairment (MCI) and Alzheimer's disease (AD)? And, do cerebrovascular and AD lesions represent additive factors in the development of MCI as a putative preclinical stage of AD? Here we reported two studies that tested these hypotheses. EEG data were recorded in normal elderly (Nold), amnesic MCI, and mild AD subjects at rest condition (closed eyes). Direction of information flow within EEG electrode pairs was performed by directed transfer function (DTF) at δ (2–4 Hz), θ (4–8 Hz), α1 (8–10 Hz), α2 (10–12 Hz), β1 (13–20 Hz), β2 (20–30 Hz), and γ (30–40 Hz). Parieto-to-frontal direction was stronger in Nold than in MCI and/or AD subjects for α and β rhythms. In contrast, the directional flow within interhemispheric EEG functional coupling did not discriminate among the groups. More interestingly, this coupling was higher at θ, α1, α2, and β1 in MCI with higher than in MCI with lower vascular load. These results suggest that directionality of parieto-to-frontal EEG synchronization is abnormal not only in AD but also in amnesic MCI, supporting the additive model according to which MCI state would result from the combination of cerebrovascular and neurodegenerative lesions.