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Electrophysiology of Alzheimer's Disease

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Dr. Marco Weiergräber

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Federal Institute for Drugs and Medical Devices (Bundesinstitut für Arzneimittel und Medizinprodukte, BfArM, Bonn, Germany
Interests: Alzheimer’s disease; brain rhythmicity; calcium channels and GABAergic system; drug treatment and regulation in Alzheimer’s disease; EEG biomarkers; EEG recording and analysis in mutant (AD) mouse models; hippocampal activity; neurodegenerative diseases; neuronal network dysfunction

Special Issue Information

Alzheimer’s disease will be one of the biggest challenges for public health systems in the future. Strong efforts in basic science are mandatory to improve our understanding of the etiopathogenesis of AD to finally improve diagnosis, treatment, and drug research and development in this field. This Special Issue focuses on a most promising approach in Alzheimer research—that is, electrophysiological alterations and their functional implications in the etiopathogenesis of the disease.

This Issue intends to provide the reader with in vitro and in vivo electrophysiological studies, particularly in AD animal models on the micro, meso, and macro scale. Methodologically, the latter include, among other things, patch-clamp and multi-electrode array (MEA) studies, electroencephalographic recordings, and evoked potentials. Studies on, for example, isolated neurons or organotypic brain slice cultures are also highly welcome.

Our Special Issue is dedicated to the analysis of AD-related brain dysrhythmia and neuronal malcommunication, hyperexcitability, and excitotoxicity. Overall, we are confident that this Special Issue on current electrophysiological aspects of AD will be of interest to the broad readership of the journal and provide substantial information covering our current knowledge on electrophysiology in AD.

Dr. Marco Weiergräber
Guest Editor

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Keywords

biomarkers
clinical trials
drug regulation
EEG analysis
epidural and deep recordings
epilepsy
in vitro and in vivo techniques
mouse models
network dysrhythmia

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Research

24 pages, 2469 KiB

Open AccessArticle

Chronic BACE-1 Inhibitor Administration in TASTPM Mice (APP KM670/671NL and PSEN1 M146V Mutation): An EEG Study

by Susanna Lopez, Claudio Del Percio, Gianluigi Forloni, Angelisa Frasca, Wilhelmus H. Drinkenburg, Roberta Lizio, Giuseppe Noce, Raffaele Ferri, Andrea Soricelli, Fabrizio Stocchi, Laura Vacca, Règis Bordet, Jill C. Richardson, Claudio Babiloni and on behalf of PharmaCog Consortium

Int. J. Mol. Sci. 2020, 21(23), 9072; https://doi.org/10.3390/ijms21239072 - 28 Nov 2020

Cited by 1 | Viewed by 2015

Abstract

Objective. In this exploratory study, we tested whether electroencephalographic (EEG) rhythms may reflect the effects of a chronic administration (4 weeks) of an anti-amyloid β-site amyloid precursor protein (APP) cleaving enzyme 1 inhibitor (BACE-1; ER-901356; Eisai Co., Ltd., Tokyo, Japan) in TASTPM (double mutation in APP KM670/671NL and PSEN1 M146V) producing Alzheimer’s disease (AD) amyloid neuropathology as compared to wild type (WT) mice. Methods. Ongoing EEG rhythms were recorded from a bipolar frontoparietal and two monopolar frontomedial (prelimbic) and hippocampal channels in 11 WT Vehicle, 10 WT BACE-1, 10 TASTPM Vehicle, and 11 TASTPM BACE-1 mice (males; aged 8/9 months old at the beginning of treatment). Normalized EEG power (density) was compared between the first day (Day 0) and after 4 weeks (Week 4) of the BACE-1 inhibitor (10 mg/Kg) or vehicle administration in the 4 mouse groups. Frequency and magnitude of individual EEG delta and theta frequency peaks (IDF and ITF) were considered during animal conditions of behaviorally passive and active wakefulness. Cognitive status was not tested. Results. Compared with the WT group, the TASTPM group generally showed a significantly lower reactivity in frontoparietal ITF power during the active over the passive condition (p < 0.05). Notably, there was no other statistically significant effect (e.g., additional electrodes, recording time, and BACE-1 inhibitor). Conclusions. The above EEG biomarkers reflected differences between the WT and TASTPM groups, but no BACE-1 inhibitor effect. The results suggest an enhanced experimental design with the use of younger mice, longer drug administrations, an effective control drug, and neuropathological amyloid markers. Full article

(This article belongs to the Special Issue Electrophysiology of Alzheimer's Disease)

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17 pages, 2588 KiB

Open AccessArticle

Functional Alterations in the Olfactory Neuronal Circuit Occur before Hippocampal Plasticity Deficits in the P301S Mouse Model of Tauopathy: Implications for Early Diagnosis and Translational Research in Alzheimer’s Disease

by Abdallah Ahnaou, Daniela Rodriguez-Manrique, Ria Biermans, Sofie Embrechts, Nikolay V. Manyakov and Wilhelmus H. Drinkenburg

Int. J. Mol. Sci. 2020, 21(15), 5431; https://doi.org/10.3390/ijms21155431 - 30 Jul 2020

Cited by 11 | Viewed by 4044

Abstract

Alzheimer’s disease (AD) is characterized by neuronal loss and impaired synaptic transmission, ultimately leading to cognitive deficits. Early in the disease, the olfactory track seems most sensitive to tauopathy, while most plasticity studies focused on the hippocampal circuits. Functional network connectivity (FC) and long-term potentiation (LTP), considered as the plasticity substrate of learning and memory, were longitudinally assessed in mice of the P301S model of tauopathy following the course (time and location) of progressively neurodegenerative pathology (i.e., at 3, 6, and 9 months of age) and in their wild type (WT) littermates. Using in vivo local field potential (LFP) recordings, early (at three months) dampening in the gamma oscillatory activity and impairments in the phase-amplitude theta-gamma coupling (PAC) were found in the olfactory bulb (OB) circuit of P301S mice, which were maintained through the whole course of pathology development. In contrast, LFP oscillatory activity and PAC indices were normal in the entorhinal cortex, hippocampal CA1 and CA3 nuclei. Field excitatory postsynaptic potential (fEPSP) recordings from the Shaffer collateral (SC)-CA1 hippocampal stratum pyramidal revealed a significant altered synaptic LTP response to high-frequency stimulation (HFS): at three months of age, no significant difference between genotypes was found in basal synaptic activity, while signs of a deficit in short term plasticity were revealed by alterations in the fEPSPs. At six months of age, a slight deviance was found in basal synaptic activity and significant differences were observed in the LTP response. The alterations in network oscillations at the OB level and impairments in the functioning of the SC-CA1 pyramidal synapses strongly suggest that the progression of tau pathology elicited a brain area, activity-dependent disturbance in functional synaptic transmission. These findings point to early major alterations of neuronal activity in the OB circuit prior to the disturbance of hippocampal synaptic plasticity, possibly involving tauopathy in the anomalous FC. Further research should determine whether those early deficits in the OB network oscillations and FC are possible mechanisms that potentially promote the emergence of hippocampal synaptic impairments during the progression of tauopathy. Full article

(This article belongs to the Special Issue Electrophysiology of Alzheimer's Disease)

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