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      Altered Theta Oscillations and Aberrant Cortical Excitatory Activity in the 5XFAD Model of Alzheimer's Disease

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          Abstract

          Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by impairment of memory function. The 5XFAD mouse model was analyzed and compared with wild-type (WT) controls for aberrant cortical excitability and hippocampal theta oscillations by using simultaneous video-electroencephalogram (EEG) monitoring. Seizure staging revealed that 5XFAD mice exhibited cortical hyperexcitability whereas controls did not. In addition, 5XFAD mice displayed a significant increase in hippocampal theta activity from the light to dark phase during nonmotor activity. We also observed a reduction in mean theta frequency in 5XFAD mice compared to controls that was again most prominent during nonmotor activity. Transcriptome analysis of hippocampal probes and subsequent qPCR validation revealed an upregulation of Plcd4 that might be indicative of enhanced muscarinic signalling. Our results suggest that 5XFAD mice exhibit altered cortical excitability, hippocampal dysrhythmicity, and potential changes in muscarinic signaling.

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          Theta oscillations in the hippocampus.

          György Buzsáki (2002)
          Theta oscillations represent the "on-line" state of the hippocampus. The extracellular currents underlying theta waves are generated mainly by the entorhinal input, CA3 (Schaffer) collaterals, and voltage-dependent Ca(2+) currents in pyramidal cell dendrites. The rhythm is believed to be critical for temporal coding/decoding of active neuronal ensembles and the modification of synaptic weights. Nevertheless, numerous critical issues regarding both the generation of theta oscillations and their functional significance remain challenges for future research.
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            Caspase signalling controls microglia activation and neurotoxicity.

            Miguel Burguillos, Tomas Deierborg, Edel Kavanagh … (2011)
            Activation of microglia and inflammation-mediated neurotoxicity are suggested to play a decisive role in the pathogenesis of several neurodegenerative disorders. Activated microglia release pro-inflammatory factors that may be neurotoxic. Here we show that the orderly activation of caspase-8 and caspase-3/7, known executioners of apoptotic cell death, regulate microglia activation through a protein kinase C (PKC)-δ-dependent pathway. We find that stimulation of microglia with various inflammogens activates caspase-8 and caspase-3/7 in microglia without triggering cell death in vitro and in vivo. Knockdown or chemical inhibition of each of these caspases hindered microglia activation and consequently reduced neurotoxicity. We observe that these caspases are activated in microglia in the ventral mesencephalon of Parkinson's disease (PD) and the frontal cortex of individuals with Alzheimer's disease (AD). Taken together, we show that caspase-8 and caspase-3/7 are involved in regulating microglia activation. We conclude that inhibition of these caspases could be neuroprotective by targeting the microglia rather than the neurons themselves.
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              A network dysfunction perspective on neurodegenerative diseases.

              Jorge Palop, Jeannie Chin, Lennart Mucke (2006)
              Patients with Alzheimer's disease or other neurodegenerative disorders show remarkable fluctuations in neurological functions, even during the same day. These fluctuations cannot be caused by sudden loss or gain of nerve cells. Instead, it is likely that they reflect variations in the activity of neural networks and, perhaps, chronic intoxication by abnormal proteins that the brain is temporarily able to overcome. These ideas have far-reaching therapeutic implications.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Neural Plast
                Journal ID (iso-abbrev): Neural Plast
                Journal ID (publisher-id): NP
                Title: Neural Plasticity
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-5904
                ISSN (Electronic): 1687-5443
                Publication date (Print): 2015
                Publication date (Electronic): 2 April 2015
                Volume: 2015
                Electronic Location Identifier: 781731
                Affiliations
                1Federal Institute for Drugs and Medical Devices (BfArM), Kurt-Georg-Kiesinger-Allee 3, 53175 Bonn, Germany
                2Department of Psychiatry and Psychotherapy, University of Cologne, Faculty of Medicine, Kerpener Street 62, 50937 Cologne, Germany
                3Institute of Molecular Psychiatry, University of Bonn, Sigmund-Freud Street 25, 53125 Bonn, Germany
                4German Center for Neurodegenerative Diseases (DZNE), Ludwig-Erhard-Allee 2, 53175 Bonn, Germany
                Author notes

                Academic Editor: Michel Baudry

                Author information
                http://orcid.org/0000-0001-7464-1335
                Article
                DOI: 10.1155/2015/781731
                PMC ID: 4398951
                PubMed ID: 25922768
                SO-VID: a0372e72-8864-4d5e-a634-bc89006276b3
                Copyright © Copyright © 2015 Magdalena Elisabeth Siwek et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 30 January 2015
                Date accepted : 18 March 2015
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Neurosciences
                Data availability:
                ScienceOpen disciplines: Neurosciences

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