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      Recurrent Epileptic Auras As a Presenting Symptom of Alzheimer’s Disease

      case-report

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          Abstract

          Seizures are a common co-morbidity during the course of Alzheimer’s disease (AD) and in a subset of patients may be one of the presenting symptoms. In this case series, we highlight three patients with recurrent medically refractory epileptic auras whose work up ultimately lead to the diagnosis of AD. All three patients underwent prolonged EEG, serial neuropsychological testing, FDG-PET, cerebrospinal fluid (CSF) AD biomarkers, and MRI. CSF biomarkers were particularly helpful in two cases. These cases highlight the importance of having a high index of suspicion for AD in new onset “idiopathic” epilepsy in the elderly.

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          Most cited references11

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          Silent Hippocampal Seizures and Spikes Identified by Foramen Ovale Electrodes in Alzheimer’s Disease

          We directly assessed mesial temporal activity in two Alzheimer’s disease (AD) patients without a history or EEG evidence of seizures, using intracranial foramen ovale electrodes. We detected clinically silent hippocampal seizures and epileptiform spikes during sleep, a period when both were most likely to interfere with memory consolidation. These index cases support a model in which early development of occult hippocampal hyperexcitability may contribute to the pathogenesis of AD.
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            Brain PET in the diagnosis of Alzheimer's disease.

            The aim of this article was to review the current role of brain PET in the diagnosis of Alzheimer dementia. The characteristic patterns of glucose metabolism on brain FDG-PET can help in differentiating Alzheimer's disease from other causes of dementia such as frontotemporal dementia and dementia of Lewy body. Amyloid brain PET may exclude significant amyloid deposition and thus Alzheimer's disease in appropriate clinical setting.
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              Tau loss attenuates neuronal network hyperexcitability in mouse and Drosophila genetic models of epilepsy.

              Neuronal network hyperexcitability underlies the pathogenesis of seizures and is a component of some degenerative neurological disorders such as Alzheimer's disease (AD). Recently, the microtubule-binding protein tau has been implicated in the regulation of network synchronization. Genetic removal of Mapt, the gene encoding tau, in AD models overexpressing amyloid-β (Aβ) decreases hyperexcitability and normalizes the excitation/inhibition imbalance. Whether this effect of tau removal is specific to Aβ mouse models remains to be determined. Here, we examined tau as an excitability modifier in the non-AD nervous system using genetic deletion of tau in mouse and Drosophila models of hyperexcitability. Kcna1(-/-) mice lack Kv1.1-delayed rectifier currents and exhibit severe spontaneous seizures, early lethality, and megencephaly. Young Kcna1(-/-) mice retained wild-type levels of Aβ, tau, and tau phospho-Thr(231). Decreasing tau in Kcna1(-/-) mice reduced hyperexcitability and alleviated seizure-related comorbidities. Tau reduction decreased Kcna1(-/-) video-EEG recorded seizure frequency and duration as well as normalized Kcna1(-/-) hippocampal network hyperexcitability in vitro. Additionally, tau reduction increased Kcna1(-/-) survival and prevented megencephaly and hippocampal hypertrophy, as determined by MRI. Bang-sensitive Drosophila mutants display paralysis and seizures in response to mechanical stimulation, providing a complementary excitability assay for epistatic interactions. We found that tau reduction significantly decreased seizure sensitivity in two independent bang-sensitive mutant models, kcc and eas. Our results indicate that tau plays a general role in regulating intrinsic neuronal network hyperexcitability independently of Aβ overexpression and suggest that reducing tau function could be a viable target for therapeutic intervention in seizure disorders and antiepileptogenesis.
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                Author and article information

                Contributors
                Journal
                Front Neurol
                Front Neurol
                Front. Neurol.
                Frontiers in Neurology
                Frontiers Media S.A.
                1664-2295
                24 July 2017
                2017
                : 8
                : 360
                Affiliations
                [1] 1Department of Neurology, Brigham and Women’s Hospital, Harvard Medical School , Boston, MA, United States
                Author notes

                Edited by: Fernando Cendes, Universidade Estadual de Campinas, Brazil

                Reviewed by: Jorge Mario Rodríguez-Fernández, University of Illinois at Chicago, United States; Stephan Schuele, Northwestern University, United States

                *Correspondence: Rani A. Sarkis, rsarkis@ 123456bwh.harvard.edu

                Specialty section: This article was submitted to Epilepsy, a section of the journal Frontiers in Neurology

                Article
                10.3389/fneur.2017.00360
                5522840
                28790971
                e6093157-f0c2-4435-b45b-2337926035d4
                Copyright © 2017 Sarkis, Willment, Gale and Dworetzky.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 16 May 2017
                : 07 July 2017
                Page count
                Figures: 1, Tables: 2, Equations: 0, References: 21, Pages: 5, Words: 3293
                Categories
                Neuroscience
                Case Report

                Neurology
                elderly,epilepsy,alzheimer’s,seizure semiology,aura
                Neurology
                elderly, epilepsy, alzheimer’s, seizure semiology, aura

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