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Action Mechanisms of Transcranial Direct Current Stimulation in Alzheimer’s Disease and Memory Loss

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      Abstract

      The pharmacological treatment of Alzheimer’s disease (AD) is often limited and accompanied by drug side effects. Thus alternative therapeutic strategies such as non-invasive brain stimulation are needed. Few studies have demonstrated that transcranial direct current stimulation (tDCS), a method of neuromodulation with consecutive robust excitability changes within the stimulated cortex area, is beneficial in AD. There is also evidence that tDCS enhances memory function in cognitive rehabilitation in depressive patients, Parkinson’s disease, and stroke. tDCS improves working and visual recognition memory in humans and object-recognition learning in the elderly. AD’s neurobiological mechanisms comprise changes in neuronal activity and the cerebral blood flow (CBF) caused by altered microvasculature, synaptic dysregulation from ß-amyloid peptide accumulation, altered neuromodulation via degenerated modulatory amine transmitter systems, altered brain oscillations, and changes in network connectivity. tDCS alters (i) neuronal activity and (ii) human CBF, (iii) has synaptic and non-synaptic after-effects (iv), can modify neurotransmitters polarity-dependently, (v) and alter oscillatory brain activity and (vi) functional connectivity patterns in the brain. It thus is reasonable to use tDCS as a therapeutic instrument in AD as it improves cognitive function in manner based on a disease mechanism. Moreover, it could prove valuable in other types of dementia. Future large-scale clinical and mechanism-oriented studies may enable us to identify its therapeutic validity in other types of demential disorders.

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      Excitability changes induced in the human motor cortex by weak transcranial direct current stimulation.

      In this paper we demonstrate in the intact human the possibility of a non-invasive modulation of motor cortex excitability by the application of weak direct current through the scalp. Excitability changes of up to 40 %, revealed by transcranial magnetic stimulation, were accomplished and lasted for several minutes after the end of current stimulation. Excitation could be achieved selectively by anodal stimulation, and inhibition by cathodal stimulation. By varying the current intensity and duration, the strength and duration of the after-effects could be controlled. The effects were probably induced by modification of membrane polarisation. Functional alterations related to post-tetanic potentiation, short-term potentiation and processes similar to postexcitatory central inhibition are the likely candidates for the excitability changes after the end of stimulation. Transcranial electrical stimulation using weak current may thus be a promising tool to modulate cerebral excitability in a non-invasive, painless, reversible, selective and focal way.
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        Neural synchrony in brain disorders: relevance for cognitive dysfunctions and pathophysiology.

        Following the discovery of context-dependent synchronization of oscillatory neuronal responses in the visual system, novel methods of time series analysis have been developed for the examination of task- and performance-related oscillatory activity and its synchronization. Studies employing these advanced techniques revealed that synchronization of oscillatory responses in the beta- and gamma-band is involved in a variety of cognitive functions, such as perceptual grouping, attention-dependent stimulus selection, routing of signals across distributed cortical networks, sensory-motor integration, working memory, and perceptual awareness. Here, we review evidence that certain brain disorders, such as schizophrenia, epilepsy, autism, Alzheimer's disease, and Parkinson's are associated with abnormal neural synchronization. The data suggest close correlations between abnormalities in neuronal synchronization and cognitive dysfunctions, emphasizing the importance of temporal coordination. Thus, focused search for abnormalities in temporal patterning may be of considerable clinical relevance.
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          Working memory

           A Baddeley (1992)
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            Author and article information

            Affiliations
            1simpleDepartment of Neurophysiology, Ruhr University Bochum Bochum, Germany
            Author notes

            Edited by: Andre R. Brunoni, Universidade de São Paulo, Brazil

            Reviewed by: Luiz Kobuti Ferreira, Universidade de Sao Paulo, Brazil; Pedro Shiozawa, Santa Casa de Misericórdia de São Paulo, Brazil

            *Correspondence: Niels Hansen, Department of Neurophysiology, Ruhr University Bochum, Universitätsstrasse 150, MA 4/150, 44780 Bochum, Germany. e-mail: niels.hansen@ 123456rub.de

            This article was submitted to Frontiers in Neuropsychiatric Imaging and Stimulation, a specialty of Frontiers in Psychiatry.

            Journal
            Front Psychiatry
            Front Psychiatry
            Front. Psychiatry
            Frontiers in Psychiatry
            Frontiers Research Foundation
            1664-0640
            15 May 2012
            2012
            : 3
            3351674
            22615703
            10.3389/fpsyt.2012.00048
            Copyright © 2012 Hansen.

            This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.

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            Figures: 0, Tables: 2, Equations: 0, References: 83, Pages: 8, Words: 6964
            Categories
            Psychiatry
            Review Article

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