EEG alterations during wake and sleep in mild cognitive impairment and Alzheimer's disease.

Patients with Alzheimer's disease (AD) undergo a slowing of waking electroencephalographic (EEG) rhythms since prodromal stages, which could be ascribed to poor sleep quality. We examined the relationship between wake and sleep alterations by assessing EEG activity during sleep and (pre-sleep/post-sleep) wakefulness in AD, mild cognitive impairment (MCI) and healthy controls. AD and MCI show high sleep latency and less slow-wave sleep.

In Search of Sleep Biomarkers of Alzheimer's Disease: K-Complexes Do Not Discriminate between Patients with Mild Cognitive Impairment and Healthy Controls.

The K-complex (KC) is one of the hallmarks of Non-Rapid Eye Movement (NREM) sleep. Recent observations point to a drastic decrease of spontaneous KCs in Alzheimer's disease (AD). However, no study has investigated when, in the development of AD, this phenomenon starts.

The Fall of Sleep K-Complex in Alzheimer Disease.

Although a slowing of electroencephalographic (EEG) activity during wakefulness and -to some extent- sleep of Alzheimer disease (AD) patients (i.e., increased slow-frequency activity) was documented, recent findings in healthy elderly show a decreased 0.

Parietal Fast Sleep Spindle Density Decrease in Alzheimer's Disease and Amnesic Mild Cognitive Impairment.

Several studies have identified two types of sleep spindles: fast (13-15 Hz) centroparietal and slow (11-13 Hz) frontal spindles. Alterations in spindle activity have been observed in Alzheimer's disease (AD) and Mild Cognitive Impairment (MCI). Only few studies have separately assessed fast and slow spindles in these patients showing a reduction of fast spindle count, but the possible local specificity of this phenomenon and its relation to cognitive decline severity are not clear.

The assessment of somatosensory cortex plasticity during sleep deprivation by paired associative stimulation.

Many animal studies suggest that during sleep deprivation (SD) synaptic strength should progressively increase, leading to the saturation of the ability to induce long-term potentiation (LTP). Nevertheless, direct evidences about the effects of sustained wakefulness on cortical plasticity in humans are still lacking. The aim of the present study was to assess changes in the ability to induce LTP-like mechanism in humans during a period of SD by means of a paired associative stimulation (PAS) protocol, which combines median nerve stimulation with transcranial magnetic stimulation (TMS) applied over the contralateral somatosensory cortex.

EEG topography during sleep inertia upon awakening after a period of increased homeostatic sleep pressure.

Objective: Behavioral and physiological indexes of high sleep inertia (SI) characterize the awakening from recovery (REC) sleep after prolonged wakefulness, but the associated electroencephalogram (EEG) topography has never been investigated. Here, we compare the EEG topography following the awakening from baseline (BSL) and REC sleep.

Methods: We have recorded the EEG waking activity of 26 healthy subjects immediately after the awakening from BSL sleep and from REC sleep following 40 h of prolonged wakefulness.

Topographic electroencephalogram changes associated with psychomotor vigilance task performance after sleep deprivation.

Objectives: The psychomotor vigilance task (PVT) is a widely used method for the assessment of vigilance after sleep deprivation (SDEP). However, the neural basis of PVT performance during SDEP has not been fully understood. In particular, no studies have investigated the possible relation between EEG topographical changes after sleep loss and PVT performance.

Sleep deprivation affects somatosensory cortex excitability as tested through median nerve stimulation.

Background: Changes of cortical excitability after sleep deprivation (SD) in humans have been investigated mostly in motor cortex, while there is little empirical evidence concerning somatosensory cortex, and its plastic changes across SD.

Objective: To assess excitability of primary somatosensory cortex (S1) and EEG voltage topographical characteristics associated with somatosensory evoked potentials (SEPs) during SD.

Methods: Across 41 h of SD, 16 healthy subjects participated in 4 experimental sessions (11.

Is sleep essential for neural plasticity in humans, and how does it affect motor and cognitive recovery?

There is a general consensus that sleep is strictly linked to memory, learning, and, in general, to the mechanisms of neural plasticity, and that this link may directly affect recovery processes. In fact, a coherent pattern of empirical findings points to beneficial effect of sleep on learning and plastic processes, and changes in synaptic plasticity during wakefulness induce coherent modifications in EEG slow wave cortical topography during subsequent sleep. However, the specific nature of the relation between sleep and synaptic plasticity is not clear yet.