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      Gamma Band Neural Stimulation in Humans and the Promise of a New Modality to Prevent and Treat Alzheimer’s Disease

      a , * , a , b , a , c , d , a , a
      Journal of Alzheimer's Disease
      IOS Press
      40 Hz, Alzheimer’s disease, gamma, neural stimulation

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          Existing treatments for Alzheimer’s disease (AD) have questionable efficacy with a need for research into new and more effective therapies to both treat and possibly prevent the condition. This review examines a novel therapeutic modality that shows promise for treating AD based on modulating neuronal activity in the gamma frequency band through external brain stimulation. The gamma frequency band is roughly defined as being between 30 Hz-100 Hz, with the 40 Hz point being of particular significance. The epidemiology, diagnostics, existing pathological models, and related current treatment targets are initially briefly reviewed. Next, the concept of external simulation triggering brain activity in the gamma band with potential demonstration of benefit in AD is introduced with reference to a recent important study using a mouse model of the disease. The review then presents a selection of relevant studies that describe the neurophysiology involved in brain stimulation by external sources, followed by studies involving application of the modality to clinical scenarios. A table summarizing the results of clinical studies applied to AD patients is also reported and may aid future development of the modality. The use of a therapy based on modulation of gamma neuronal activity represents a novel non-invasive, non-pharmacological approach to AD. Although use in clinical scenarios is still a relatively recent area of research, the technique shows good signs of efficacy and may represent an important option for treating AD in the future.

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          Most cited references123

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          The diagnosis of dementia due to Alzheimer's disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease

          The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of revising the 1984 criteria for Alzheimer's disease (AD) dementia. The workgroup sought to ensure that the revised criteria would be flexible enough to be used by both general healthcare providers without access to neuropsychological testing, advanced imaging, and cerebrospinal fluid measures, and specialized investigators involved in research or in clinical trial studies who would have these tools available. We present criteria for all-cause dementia and for AD dementia. We retained the general framework of probable AD dementia from the 1984 criteria. On the basis of the past 27 years of experience, we made several changes in the clinical criteria for the diagnosis. We also retained the term possible AD dementia, but redefined it in a manner more focused than before. Biomarker evidence was also integrated into the diagnostic formulations for probable and possible AD dementia for use in research settings. The core clinical criteria for AD dementia will continue to be the cornerstone of the diagnosis in clinical practice, but biomarker evidence is expected to enhance the pathophysiological specificity of the diagnosis of AD dementia. Much work lies ahead for validating the biomarker diagnosis of AD dementia. Copyright © 2011. Published by Elsevier Inc.
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              The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics.

              It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer's disease (AD) may be caused by deposition of amyloid beta-peptide (Abeta) in plaques in brain tissue. According to the amyloid hypothesis, accumulation of Abeta in the brain is the primary influence driving AD pathogenesis. The rest of the disease process, including formation of neurofibrillary tangles containing tau protein, is proposed to result from an imbalance between Abeta production and Abeta clearance.

                Author and article information

                Role: Handling Associate Editor
                J Alzheimers Dis
                J. Alzheimers Dis
                Journal of Alzheimer's Disease
                IOS Press (Nieuwe Hemweg 6B, 1013 BG Amsterdam, The Netherlands )
                19 July 2018
                21 August 2018
                : 65
                : 2
                : 363-392
                [a ]Translational Medical Device Lab, National University of Ireland Galway , Galway, Ireland
                [b ]College of Medicine, Nursing and Health Science, National University of Ireland Galway , Galway, Ireland
                [c ]Department of Computer Science & Applied Physics, Galway-Mayo Institute of Technology , Galway, Ireland
                [d ]Centre for Astronomy, School of Physics, National University of Ireland Galway , Galway, Ireland
                Author notes
                [* ]Correspondence to: Barry McDermott, Translational Medical Device Lab, 2nd Floor Lambe Translational Research Facility, University Hospital Galway H91 TK33, Ireland. E-mail: b.mcdermott3@ 123456nuigalway.ie .
                © 2018 – IOS Press and the authors. All rights reserved

                This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial (CC BY-NC 4.0) License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                : 2 July 2018

                40 hz,alzheimer’s disease,gamma,neural stimulation
                40 hz, alzheimer’s disease, gamma, neural stimulation


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