Cortical Sources of Resting State EEG Rhythms are Sensitive to the Progression of Alzheimer's Disease at Early Stage.

Author: Babiloni C, Lizio R, Del Percio C, Marzano N, Soricelli A, Salvatore E, Ferri R, Cosentino FI, Tedeschi G, Montella P, Marino S, De Salvo S, Rodriguez G, Nobili F, Vernieri F, Ursini F, Mundi C, Richardson JC, Frisoni GB, Rossini PM.
Department of Molecular Medicine, University of Rome "Sapienza", Rome, Italy IRCCS San Raffaele Pisana, Roma, Italy.
Conference/Journal: J Alzheimers Dis.
Date published: 2013 Jan 22
Other: Word Count: 240

Cortical sources of resting state electroencephalographic (EEG) rhythms are abnormal in subjects with Alzheimer's disease (AD). Here we tested the hypothesis that these sources are also sensitive to the progression of early stage AD over the course of one year. The resting state eyes-closed EEG data were recorded in 88 mild AD patients at baseline (Mini Mental State Evaluation, MMSE I = 21.7 ± 0.2 standard error, SE) and at approximately one-year follow up (13.3 months ± 0.5 SE; MMSE II = 20 ± 0.4 SE). All patients received standard therapy with acetylcholinesterase inhibitors. EEG recordings were also performed in 35 normal elderly (Nold) subjects as controls. EEG rhythms of interest were delta (2-4 Hz), theta (4-8 Hz), alpha 1 (8-10.5 Hz), alpha 2 (10.5-13 Hz), beta 1 (13-20 Hz), beta 2 (20-30 Hz), and gamma (30-40 Hz). Cortical EEG sources were estimated by low-resolution brain electromagnetic tomography (LORETA). Compared to the Nold subjects, the mild AD patients were characterized by a power increase of widespread delta sources and by a power decrease of posterior alpha sources. In the mild AD patients, the follow-up EEG recordings showed increased power of widespread delta sources as well as decreased power of widespread alpha and posterior beta 1 sources. These results suggest that the resting state EEG sources were sensitive, at least at group level, to the cognitive decline occurring in the mild AD group over a one-year period, and might represent cost-effective and non-invasive markers with which to enrich cohorts of AD patients that decline faster for clinical studies.
PMID: 23340039