Objective: A relationship between brain atrophy and delta rhythmicity (1.5–4 Hz) has been previously explored in Alzheimer’s disease (AD) subjects [Fernandez A, Arrazola J, Maestu F, Amo C, Gil-Gregorio P, Wienbruch C, Ortiz T. Correlations of hippocampal atrophy and focal low-frequency magnetic activity in Alzheimer disease: volumetric MR imaging-magnetoencephalographic study. Am J Neuroradiol. 2003 24(3):481–487]. In this study, we tested the hypothesis that such a relationship does exist not only in AD patients but also across the continuum of subjects with mild cognitive impairment (MCI) and AD. Methods: Resting, eyes-closed EEG data were recorded in 34 MCI and 65 AD subjects. 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), and beta 2 (20–30 Hz). EEG cortical sources were estimated by LORETA. Cortical EEG sources were correlated with MR-based measurements of lobar brain volume (white and gray matter). Results: A negative correlation was observed between the frontal white matter and the amplitude of frontal delta sources (2–4 Hz) across MCI and AD subjects. Conclusions: These results confirmed for the first time the hypothesis that the sources of resting delta rhythms (2–4 Hz) are correlated with lobar brain volume across MCI and AD subjects. Significance: The present findings support, at least at group level, the ‘transition hypothesis’ of brain structural and functional continuity between MCI and AD.

Frontal white matter volume and delta EEG sorces negatively correlate in awake subjects with mild cognitive impairment and Alzheimer’s disease / C., Babiloni; G. B., Frisoni; M., Steriade; L., Bresciani; G., Binetti; C., Del Percio; C., Geroldi; Miniussi, Carlo; F., Nobili; G., Rodriguez; F., Zappasodi; T., Carfagna; P. M., Rossini. - In: CLINICAL NEUROPHYSIOLOGY. - ISSN 1388-2457. - 2006:5(2006), pp. 1113-1129. [10.1016/j.clinph.2006.01.020]

Frontal white matter volume and delta EEG sorces negatively correlate in awake subjects with mild cognitive impairment and Alzheimer’s disease.

Miniussi, Carlo;
2006-01-01

Abstract

Objective: A relationship between brain atrophy and delta rhythmicity (1.5–4 Hz) has been previously explored in Alzheimer’s disease (AD) subjects [Fernandez A, Arrazola J, Maestu F, Amo C, Gil-Gregorio P, Wienbruch C, Ortiz T. Correlations of hippocampal atrophy and focal low-frequency magnetic activity in Alzheimer disease: volumetric MR imaging-magnetoencephalographic study. Am J Neuroradiol. 2003 24(3):481–487]. In this study, we tested the hypothesis that such a relationship does exist not only in AD patients but also across the continuum of subjects with mild cognitive impairment (MCI) and AD. Methods: Resting, eyes-closed EEG data were recorded in 34 MCI and 65 AD subjects. 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), and beta 2 (20–30 Hz). EEG cortical sources were estimated by LORETA. Cortical EEG sources were correlated with MR-based measurements of lobar brain volume (white and gray matter). Results: A negative correlation was observed between the frontal white matter and the amplitude of frontal delta sources (2–4 Hz) across MCI and AD subjects. Conclusions: These results confirmed for the first time the hypothesis that the sources of resting delta rhythms (2–4 Hz) are correlated with lobar brain volume across MCI and AD subjects. Significance: The present findings support, at least at group level, the ‘transition hypothesis’ of brain structural and functional continuity between MCI and AD.
2006
5
C., Babiloni; G. B., Frisoni; M., Steriade; L., Bresciani; G., Binetti; C., Del Percio; C., Geroldi; Miniussi, Carlo; F., Nobili; G., Rodriguez; F., Z...espandi
Frontal white matter volume and delta EEG sorces negatively correlate in awake subjects with mild cognitive impairment and Alzheimer’s disease / C., Babiloni; G. B., Frisoni; M., Steriade; L., Bresciani; G., Binetti; C., Del Percio; C., Geroldi; Miniussi, Carlo; F., Nobili; G., Rodriguez; F., Zappasodi; T., Carfagna; P. M., Rossini. - In: CLINICAL NEUROPHYSIOLOGY. - ISSN 1388-2457. - 2006:5(2006), pp. 1113-1129. [10.1016/j.clinph.2006.01.020]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11572/145584
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