Ciro Mundi

Occipital sources of resting-state alpha rhythms are related to local gray matter density in subjects with amnesic mild cognitive impairment and Alzheimer's disease

Occipital sources of resting-state electroencephalographic (EEG) alpha rhythms are abnormal, at the group level, in patients with amnesic mild cognitive impairment (MCI) and Alzheimers disease (AD). Here, we evaluated the hypothesis that amplitude of these occipital sources is related to neurodegeneration in occipital lobe as measured by magnetic resonance imaging. Resting-state eyes-closed EEG rhythms were recorded in 45 healthy elderly (Nold), 100 MCI, and 90 AD subjects. Neurodegeneration of occipital lobe was indexed by weighted averages of gray matter density, estimated from structural MRIs. EEG rhythms of interest were alpha 1 (8-10.5 Hz) and alpha 2 (10.5-13 Hz). EEG cortical sources were estimated by low-resolution brain electromagnetic tomography. Results showed a positive correlation between occipital gray matter density and amplitude of occipital alpha 1 sources in Nold, MCI, and AD subjects as a whole group (r = 0.3, p = 0.000004, N = 235). Furthermore, there was a positive correlation between the amplitude of occipital alpha 1 sources and cognitive status as revealed by Mini Mental State Examination score across all subjects (r = 0.38, p = 0.000001, N = 235). Finally, amplitude of occipital alpha 1 sources allowed a moderate classification of individual Nold and AD subjects (sensitivity: 87.8%; specificity: 66.7%; area under the receiver operating characteristic curve: 0.81). These results suggest that the amplitude of occipital sources of resting-state alpha rhythms is related to AD neurodegeneration in occipital lobe along pathologic aging.

Resting State Cortical Electroencephalographic Rhythms and White Matter Vascular Lesions in Subjects with Alzheimer's Disease: An Italian Multicenter Study

Resting state electroencephalographic (EEG) rhythms do not deteriorate with the increase of white matter vascular lesion in amnesic mild cognitive impairment (MCI) subjects [1], although white matter is impaired along Alzheimers disease (AD). Here we tested whether this is true even in AD subjects. Closed-eye resting state EEG data were recorded in 40 healthy elderly (Nold), 96 amnesic MCI, and 83 AD subjects. White matter vascular lesions were indexed by magnetic resonance imaging recorded in the MCI and AD subjects (about 42% of cases following ADNI standards). The MCI subjects were divided into two sub-groups based on the median of the white matter lesion, namely MCI+ (people with highest vascular load; n = 48) and MCI- (people with lowest vascular load; n = 48). The same was true for the AD subjects (AD+, n = 42; AD-, n = 41). EEG rhythms of interest were delta (2-4 Hz), theta (4-8 Hz), alpha1 (8-10.5 Hz), alpha2 (10.5-13 Hz), beta1 (13-20 Hz), beta2 (20-30 Hz), and gamma (30-40 Hz). LORETA software estimated cortical EEG sources. When compared to Nold group, MCI and AD groups showed well known abnormalities of delta and alpha sources. Furthermore, amplitude of occipital, temporal, and limbic alpha 1 sources were higher in MCI+ than MCI- group. As a novelty, amplitude of occipital delta sources was lower in AD+ than AD- group. Furthermore, central, parietal, occipital, temporal, and limbic alpha sources were higher in amplitude in AD+ than AD- group. Amplitude of these sources was correlated to global cognitive status (i.e., Mini Mental State Evaluation score). These results suggest that in amnesic MCI and AD subjects, resting state posterior delta and alpha EEG rhythms do not deteriorate with the increase of white-matter vascular lesion. These rhythms might be more sensitive to AD neurodegenerative processes and cognitive status rather than to concomitant lesions to white matter.

Cortical sources of resting state EEG rhythms are sensitive to the progression of early stage Alzheimer's disease

Cortical sources of resting state electroencephalographic (EEG) rhythms are abnormal in subjects with Alzheimers 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.

Cortical sources of resting state electroencephalographic alpha rhythms deteriorate across time in subjects with amnesic mild cognitive impairment

Cortical sources of resting state electroencephalographic (EEG) rhythms are abnormal in subjects with mild cognitive impairment (MCI). Here, we tested the hypothesis that these sources in amnesic MCI subjects further deteriorate over 1 year. To this aim, the resting state eyes-closed EEG data were recorded in 54 MCI subjects at baseline (Mini Mental State Examination I = 26.9; standard error [SE], 0.2) and at approximately 1-year follow-up (13.8 months; SE, 0.5; Mini Mental State Examination II = 25.8; SE, 0.2). As a control, EEG recordings were also performed in 45 normal elderly and in 50 mild Alzheimers disease subjects. EEG rhythms of interest were delta (2-4 Hz), theta (4-8 Hz), alpha1 (8-10.5 Hz), alpha2 (10.5-13 Hz), beta1 (13-20 Hz), and beta2 (20-30 Hz). Cortical EEG sources were estimated using low-resolution brain electromagnetic tomography. Compared with the normal elderly and mild Alzheimers disease subjects, the MCI subjects were characterized by an intermediate power of posterior alpha1 sources. In the MCI subjects, the follow-up EEG recordings showed a decreased power of posterior alpha1 and alpha2 sources. These results suggest that the resting state EEG alpha sources were sensitive-at least at the group level-to the cognitive decline occurring in the amnesic MCI group over 1 year, and might represent cost-effective, noninvasive and widely available markers to follow amnesic MCI populations in large clinical trials.

Resting state Rolandic mu rhythms are related to activity of sympathetic component of autonomic nervous system in healthy humans

We tested the hypothesis of a relationship between heart rate variability (HRV) and Rolandic mu rhythms in relaxed condition of resting state. Resting state eyes-closed electroencephalographic (EEG) and electrocardiographic (ECG) data were recorded (10-20 System) in 42 healthy adults. EEG rhythms of interest were high-frequency alpha (10.5-13Hz) and low-frequency beta (13-20Hz), which are supposed to form Rolandic mu rhythms. Rolandic and occipital (control) EEG sources were estimated by LORETA software. Results showed a statistically significant (p<0.05, corrected) negative correlation across all subjects between Rolandic cortical sources of low-frequency beta rhythms and the low-frequency band power (LF, 0.04-0.15Hz) of tachogram spectrum as an index of HRV. The lower the amplitude of Rolandic sources of low-frequency beta rhythms (as a putative sign of activity of somatomotor cortex), the higher the LF band power of tachogram spectrum (as a putative sign of sympathetic activity). This effect was specific as there was neither a similar correlation between these EEG rhythms and high-frequency band power of tachogram spectrum (as a putative sign of parasympathetic vagal activity) neither between occipital sources of low-frequency beta rhythms (as a putative sign of activity of visual cortex) and LF band power of tachogram spectrum. These results suggest that Rolandic low-frequency beta rhythms are related to sympathetic activity regulating heart rate, as a dynamic neurophysiologic oscillatory mechanism sub-serving the interaction between brain neural populations involved in somatomotor control and brain neural populations regulating ANS signals to heart for on-going homeostatic adaptations.

Resting state cortical electroencephalographic rhythms in subjects with normal and abnormal body weight

It is well known that resting state regional cerebral blood flow is abnormal in obese when compared to normal-weight subjects but the underlying neurophysiological mechanisms are poorly known. To address this issue, we tested the hypothesis that amplitude of resting state cortical electroencephalographic (EEG) rhythms differ among underweight, normal-weight, and overweight/obese subjects as a reflection of the relationship between cortical neural synchronization and regulation of body weight. Eyes-closed resting state EEG data were recorded in 16 underweight subjects, 25 normal-weight subjects, and 18 overweight/obese subjects. All subjects were psychophysically healthy (no eating disorders or major psychopathologies). EEG rhythms of interest were delta (2-4Hz), theta (4-8Hz), alpha 1 (8-10.5Hz), alpha 2 (10.5-13Hz), beta 1 (13-20Hz), beta 2 (20-30Hz), and gamma (30-40Hz). EEG cortical sources were estimated by low-resolution brain electromagnetic tomography (LORETA). Statistical results showed that parietal and temporal alpha 1 sources fitted the pattern underweight>normal-weight>overweight/obese (p<0.004), whereas occipital alpha 1 sources fitted the pattern normal-weight>underweight>overweight/obese (p<0.00003). Furthermore, amplitude of the parietal, occipital, and temporal alpha 2 sources was stronger in the normal-weight subjects than in the underweight and overweight/obese subjects (p<0.0007). These results suggest that abnormal weight in healthy overweight/obese subjects is related to abnormal cortical neural synchronization at the basis of resting state alpha rhythms and fluctuation of global brain arousal.

Poor desynchronisation of resting-state eyes-open cortical alpha rhythms in obese subjects without eating disorders

OBJECTIVE Obese subjects without eating disorders were characterised by poor electroencephalographic (EEG) alpha rhythms during resting-state eye-closed condition (Babiloni et al., 2011b). Is this true also for the desynchronisation of alpha rhythms during resting-state eyes opening? METHODS EEG data were recorded in 15 underweight, 20 normal-weight, and 18 overweight/obese subjects during resting-state eyes-closed and -open conditions. EEG sources were estimated by LORETA for alpha 1 (8-10.5 Hz) and alpha 2 (10.5-13 Hz). The alpha desynchronisation was calculated as the difference eyes-open minus -closed condition. RESULTS The occipital alpha 1 desynchronisation was lower in overweight/obese and underweight subjects compared with normal-weight subjects (p < 0.000005). The same was true for parietal, occipital and temporal alpha 2 (10.5-13 Hz) desynchronisation (p < 0.000002). The parietal and temporal alpha 1 desynchronisation was lower in overweight/obese than in normal-weight subjects (p < 0.00001). These effects spatially matched those observed in the resting-state eyes-closed condition. CONCLUSION Subjects with abnormal weight and normal eating behaviour are characterised by poor alpha desynchronisation during resting-state eyes opening. SIGNIFICANCE Obese subjects without eating disorders show abnormal mechanisms of cortical neural synchronisation and desynchronisation of alpha rhythms in the resting state condition.

65. Cortical sources of resting state EEG rhythms reflect disease progression over 1 year in mild cognitive impairment and Alzheimer’s disease patients

Cortical sources of resting state electroencephalographic (EEG) rhythms are abnormal in subjects with mild cognitive impairment (MCI) and in patients with Alzheimer’s disease (AD). Here, we tested the hypothesis that they reflect disease progression for future clinical trials. Resting state eyes-closed EEG data were recorded in 54 amnesic MCI subjects and in 88 mild AD patients at baseline and at 1-year follow up. LORETA was used for data analysis. 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 ( p p Cortical sources of resting state EEG rhythms may be used as secondary “surrogate” end points for drug discovery in prodromal and manifest AD patients.