Motor cortex excitability in Alzheimer's disease: A transcranial magnetic stimulation study

Ferreri, Florinda; Pauri, Flavia; Pasqualetti, Patrizio; Fini, Rita; Forno, Gloria Dal; Rossini, Paolo Maria

doi:10.1002/ana.10416

Cited by 204 publications

(152 citation statements)

References 46 publications

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“…This possible explanation is in line with previous evidence of abnormal central EEG rhythms or evoked potentials in AD subjects performing voluntary movements or perceiving somatosensory stimuli (Babiloni et al, 2000;Ferri et al, 1996). Furthermore, abnormally hyperexcitable primary motor cortex has been recently reported in AD, as revealed by EEG rhythms related to self-paced movements and transcranial magnetic stimulation (Babiloni et al, 2000;Pennisi et al, 2002;Ferreri et al, 2003;).…”

Section: Relative Power and Frequency Of Alpha Rhythms In Mild Dementiasupporting

confidence: 89%

Individual analysis of EEG frequency and band power in mild Alzheimer's disease

Moretti

Babiloni

Binetti

et al. 2004

Clinical Neurophysiology

337

251

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Objective: This EEG study investigates the role of the cholinergic system, cortico-cortical connections, and sub-cortical white matter on the relationship between individual EEG frequencies and their relative power bands.Methods: EEGs were recorded at rest in 30 normal elderly subjects (Nold), 60 mild Alzheimer disease (AD) and 20 vascular dementia (VaD) patients, comparable for Mini Mental State Evaluation scores . Individual EEG frequencies were indexed by the theta/alpha transition frequency (TF) and by the individual alpha frequency (IAF) with power peak in the extended alpha range (5 -14 Hz). Relative power was separately computed for delta, theta, alpha1, alpha2, and alpha3 bands, on the basis of the TF and IAF.Results: Using normal subjects as a reference, VaD patients showed 'slowing' of alpha frequency (TF-IAF) and lower alpha2 power; Mild AD patients showed lower alpha2 and alpha3 power; delta power was higher in both AD and VaD patients; Theta power was higher only in VaD patients.Conclusions: Individual analysis of the alpha frequency and power can discriminate mild AD from VaD and normal elderly subjects.Significance: This analysis may probe pathophysiological mechanisms causing AD and VaD.

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Section: Relative Power and Frequency Of Alpha Rhythms In Mild Dementiasupporting

confidence: 89%

Individual analysis of EEG frequency and band power in mild Alzheimer's disease

Moretti

Babiloni

Binetti

et al. 2004

Clinical Neurophysiology

337

251

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“…Recent postmortem data from subjects -who had been prospectively followed and clinically characterized up to immediately before their death -indicate that hippocampal choline acetyltransferase levels are reduced in Alzheimer's dementia, but in fact they are upregulated in MCI (Lavenex and Amaral, 2000;DeKosky et al, 2002), presumably because of reactive upregulations of the enzyme activity in the unaffected hippocampal cholinergic axons. Previous EEG studies (Babiloni et al, 2000;Jelic et al, 2000Jelic et al, , 1996Ferreri et al, 2003) have shown a decrease -ranging from 8 to 10.5 Hz (low alpha) -of the alpha frequency power band in MCI subjects, when compared to normal elderly controls (Zappoli et al, 1995;Huang et al, 2000;Jelic et al, 2000;Koenig et al, 2005;Babiloni et al, 2006a). However, a recent study has shown an increase -ranging from 10.5 to 13 Hz (high alpha) -of the alpha frequency power band, on the occipital region in MCI subjects, when compared to normal elderly and AD patients (Babiloni et al, 2006a).…”

Section: Introductionmentioning

confidence: 94%

Hippocampal atrophy and EEG markers in subjects with mild cognitive impairment

Moretti

Miniussi

Frisoni

et al. 2007

Clinical Neurophysiology

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Objective: The present study evaluates the potential relationship between hippocampal atrophy and EEG brain rhythmicity, as assessed by relative band power and alpha frequency indices in a cohort of subjects with mild cognitive impairment (MCI). Methods: Eighty-eight subjects falling within the definition of MCI patients were enrolled. All subjects underwent EEG recording and magnetic resonance imaging (MRI). Volumetric morphometry estimates of the hippocampal region were computed. Individual EEG frequencies were indexed by the theta/alpha transition frequency (TF) and the individual alpha frequency (IAF). The relative power was separately computed for delta, theta, alpha1, alpha2 and alpha3 frequency bands. The MCI cohort was classified into four subgroups, based on the mean and standard deviations of the hippocampal volume of a normal elderly control sample. Results: The group with moderate hippocampal atrophy showed the highest increase in the theta power on frontal regions, and of the alpha2 and alpha3 powers on frontal and temporo-parietal areas. The analysis of the individual alpha frequency markers showed that the values for the alpha markers were highest in the group with the smallest hippocampal volume, whereas in the group with moderate hippocampal atrophy, these values were lower than in the group with severe atrophy. Conclusions: The relationship between hippocampal atrophy and EEG activity changes in MCI subjects is not proportional to the hippocampal atrophy. Therefore, EEG markers could represent a new tool for differential diagnosis. Significance: The hippocampal atrophy induces different brain synchronization/desynchronization patterns. EEG changes model the brain activity induced by a discrete change of the hippocampal volume. The changes in the EEG rhythmicity differ greatly from those in MCI patients with subcortical vascular damage.

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“…In AD patients, motor cortex excitability is increased (Ferreri et al, 2003). Extracellular A␤ enhances release probability at hippocampal synapses, increasing neuron network activity in vitro (Abramov et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Suppression of a Neocortical Potassium Channel Activity by Intracellular Amyloid-β and Its Rescue with Homer1a

Yamamoto¹,

Ueta²,

Wang³

et al. 2011

J. Neurosci.

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It is proposed that intracellular amyloid-␤ (A␤), before extracellular plaque formation, triggers cognitive deficits in Alzheimer disease (AD). Here we report how intracellular A␤ affects neuronal properties. This was done by injecting A␤ protein into rat and mouse neocortical pyramidal cells through whole-cell patch pipettes and by using 3xTg AD model mice, in which intracellular A␤ is accumulated innately. In rats, intracellular application of a mixed A␤ 1-42 preparation containing both oligomers and monomers, but not a monomeric preparation of A␤ 1-40 , broadened spike width and augmented Ca 2ϩ influx via voltage-dependent Ca 2ϩ channels in neocortical neurons. Both effects were mimicked and occluded by charybdotoxin, a blocker of large-conductance Ca 2ϩ -activated K ϩ (BK) channels, and blocked by isopimaric acid, a BK channel opener. Surprisingly, augmented Ca 2ϩ influx was caused by elongated spike duration, but not attributable to direct Ca 2ϩ channel modulation by A␤ 1-42 . The A␤ 1-42 -induced spike broadening was blocked by electroconvulsive shock (ECS), which we previously showed to facilitate BK channel opening via expression of the scaffold protein Homer1a. In young 3xTg and wild mice, we confirmed spike broadening by A␤ 1-42 , which was again mimicked and occluded by charybdotoxin and blocked by ECS. In Homer1a knock-out mice, ECS failed to block the A␤ 1-42 effect. Single-channel recording on BK channels supported these results. These findings suggest that the suppression of BK channels by intracellular A␤ 1-42 is a possible key mechanism for early dysfunction in the AD brain, which may be counteracted by activity-dependent expression of Homer1a.

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Motor cortex excitability in Alzheimer's disease: A transcranial magnetic stimulation study

Cited by 204 publications

References 46 publications

Individual analysis of EEG frequency and band power in mild Alzheimer's disease

Individual analysis of EEG frequency and band power in mild Alzheimer's disease

Hippocampal atrophy and EEG markers in subjects with mild cognitive impairment

Suppression of a Neocortical Potassium Channel Activity by Intracellular Amyloid-β and Its Rescue with Homer1a

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