Discrete wavelet transform EEG features of Alzheimer'S disease in activated states.

In this study, electroencephalogram (EEG) signals obtained by a single-electrode device from 24 subjects - 10 with Alzheimer's disease (AD) and 14 age-matched Controls (CN) - were analyzed using Discrete Wavelet Transform (DWT). The focus of the study is to determine the discriminating EEG features of AD patients while subjected to cognitive and auditory tasks, since AD is characterized by progressive impairments in cognition and memory. At each recording block, DWT extracts EEG features corresponding to major brain frequency bands. T-test and Kruskal-Wallis methods were used to determine the statistically significant features of EEG signals from AD patients compared to Controls. A decision tree algorithm was then used to identify the dominant features for AD patients. It was determined that the mean value of the low-δ (1 - 2 Hz) frequency band during the Paced Auditory Serial Addition Test with 2.0 (s) interval and the mean value of the δ frequency band (12 - 30 Hz) during 6 Hz auditory stimulation have higher mean values in AD patients than Controls. Due to artifacts, the less reliable low-δ features were removed and it was determined that the mean value of ß frequency band during 6 Hz auditory stimulation followed by the standard deviation of θ (4 - 8 Hz) frequency band of one card learning cognitive task are higher for AD patients compared to Controls and thus the most dominant discriminating features of the disease.

A matter of focus: monoaminergic modulation of stimulus coding in mammalian sensory networks.

Although the presence of neuromodulators in mammalian sensory systems has been noted for some time, a groundswell of evidence has now begun to document the scope of these regulatory mechanisms in several sensory systems, highlighting the importance of neuromodulation in shaping feature extraction at all levels of neural processing. The emergence of more sophisticated models of sensory encoding and of the interaction between sensory and regulatory regions of the brain will challenge sensory neurobiologists to further incorporate a concept of sensory network function that is contingent on neuromodulatory and behavioral state.

Norepinephrine exhibits two distinct profiles of action on sensory cortical neuron responses to excitatory synaptic stimuli.

Located within the central gray of the caudal pons, the locus coeruleus (LC) is the sole source of norepinephrine (NE) projections to the forebrain. NE is released both tonically and phasically from axonal varicosities in LC efferent target circuits. NE has been shown to produce a diverse set of actions, including suppression of spontaneous and stimulus evoked discharge, augmentation of synaptically evoked excitation, and inhibition and gating of otherwise subthreshold synaptic inputs. Utilizing an extracellular in vitro tissue slice preparation and microiontophoretic techniques, the dose-dependent actions of NE on glutamate-evoked discharges of layer II/III and layer V sensory cortical neurons were investigated. Noradrenergic effects were further examined in terms of cell and adrenoceptor specificity. The results indicate two exclusive modulatory actions of NE: 1) ejection current-dependent suppression of glutamate evoked discharge, and 2) ejection current-dependent facilitation of glutamate-evoked discharge followed by suppression of the maximal facilitated response. These effects were observed in both normal and low Ca(2+) / high Mg(2+) bathing media, suggesting a postsynaptic site for NE's actions. The facilitation of glutamate evoked discharge was selectively mimicked by the alpha-1 agonist, phenylephrine, whereas the dose-dependent suppression was mimicked by the beta-agonist isoproterenol. These results suggest that the suppressant and facilitating actions of NE are mediated by beta and alpha-1 receptors, respectively. In general, these results are consistent with previous demonstrations of NE modulatory actions on central neurons, but indicate that in the cerebral cortex these effects are both cell- and receptor-specific.