What electrophysiology tells us about Alzheimer's disease : a window into the synchronization and connectivity of brain neurons

Babiloni, Claudio and Blinowska, Katarzyna and Bonanni, Laura and Cichocki, Andrej and De Haan, Willem and Del Percio, Claudio and Dubois, Bruno and Escudero, Javier and Fernández, Alberto and Frisoni, Giovanni and Guntekin, Bahar and Hajos, Mihaly and Hampel, Harald and Ifeachor, Emmanuel and Kilborn, Kerry and Kumar, Sanjeev and Johnsen, Kristinn and Johannsson, Magnus and Jeong, Jaeseung and LeBeau, Fiona and Lizio, Roberta and Lopes da Silva, Fernando and Maestú, Fernando and McGeown, William J. and McKeith, Ian and Moretti, Davide Vito and Nobili, Flavio and Olichney, John and Onofrj, Marco and Palop, Jorge J. and Rowan, Michael and Stocchi, Fabrizio and Struzik, Zbigniew M. and Tanila, Heikki and Teipel, Stefan and Taylor, John Paul and Weiergräber, Marco and Yener, Gorsev and Young-Pearse, Tracy and Drinkenburg, Wilhelmus H. and Randall, Fiona (2020) What electrophysiology tells us about Alzheimer's disease : a window into the synchronization and connectivity of brain neurons. Neurobiology of Aging, 85. pp. 58-73. ISSN 0197-4580 (https://doi.org/10.1016/j.neurobiolaging.2019.09.0...)

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Abstract

Electrophysiology provides a real-time readout of neural functions and network capability in different brain states, on temporal (fractions of milliseconds) and spatial (micro, meso, and macro) scales unmet by other methodologies. However, current international guidelines do not endorse the use of electroencephalographic (EEG)/magnetoencephalographic (MEG) biomarkers in clinical trials performed in patients with Alzheimer's disease (AD), despite a surge in recent validated evidence. This position paper of the ISTAART Electrophysiology Professional Interest Area endorses consolidated and translational electrophysiological techniques applied to both experimental animal models of AD and patients, to probe the effects of AD neuropathology (i.e., brain amyloidosis, tauopathy, and neurodegeneration) on neurophysiological mechanisms underpinning neural excitation/inhibition and neurotransmission as well as brain network dynamics, synchronization, and functional connectivity, reflecting thalamocortical and corticocortical residual capacity. Converging evidence shows relationships between abnormalities in EEG/MEG markers and cognitive deficits in groups of AD patients at different disease stages. The supporting evidence for the application of electrophysiology in AD clinical research as well as drug discovery pathways warrants an international initiative to include the use of EEG/MEG biomarkers in the main multicentric projects planned in AD patients, to produce conclusive findings challenging the present regulatory requirements and guidelines for AD studies.

ORCID iDs

Babiloni, Claudio, Blinowska, Katarzyna, Bonanni, Laura, Cichocki, Andrej, De Haan, Willem, Del Percio, Claudio, Dubois, Bruno, Escudero, Javier, Fernández, Alberto, Frisoni, Giovanni, Guntekin, Bahar, Hajos, Mihaly, Hampel, Harald, Ifeachor, Emmanuel, Kilborn, Kerry, Kumar, Sanjeev, Johnsen, Kristinn, Johannsson, Magnus, Jeong, Jaeseung, LeBeau, Fiona, Lizio, Roberta, Lopes da Silva, Fernando, Maestú, Fernando, McGeown, William J. ORCID logoORCID: https://orcid.org/0000-0001-7943-5901, McKeith, Ian, Moretti, Davide Vito, Nobili, Flavio, Olichney, John, Onofrj, Marco, Palop, Jorge J., Rowan, Michael, Stocchi, Fabrizio, Struzik, Zbigniew M., Tanila, Heikki, Teipel, Stefan, Taylor, John Paul, Weiergräber, Marco, Yener, Gorsev, Young-Pearse, Tracy, Drinkenburg, Wilhelmus H. and Randall, Fiona;
CORE (COnnecting REpositories)