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

      research-article
      Author(s): , M.D., Ph.D 1 , , M.D. 1 , , M.D., Ph.D 2 , , M.D. 3 , , M.D., Ph.D. 2 , , M.D. 1
      Publication date (Electronic):
      Journal: Nature medicine

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          Abstract

          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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          Frequent amyloid deposition without significant cognitive impairment among the elderly.

          Howard Aizenstein, Robert Nebes, Judith Saxton … (2008)
          To characterize the prevalence of amyloid deposition in a clinically unimpaired elderly population, as assessed by Pittsburgh Compound B (PiB) positron emission tomography (PET) imaging, and its relationship to cognitive function, measured with a battery of neuropsychological tests. Subjects underwent cognitive testing and PiB PET imaging (15 mCi for 90 minutes with an ECAT HR+ scanner). Logan graphical analysis was applied to estimate regional PiB retention distribution volume, normalized to a cerebellar reference region volume, to yield distribution volume ratios (DVRs). University medical center. From a community-based sample of volunteers, 43 participants aged 65 to 88 years who did not meet diagnostic criteria for Alzheimer disease or mild cognitive impairment were included. Regional PiB retention and cognitive test performance. Of 43 clinically unimpaired elderly persons imaged, 9 (21%) showed evidence of early amyloid deposition in at least 1 brain area using an objectively determined DVR cutoff. Demographic characteristics did not differ significantly between amyloid-positive and amyloid-negative participants, and neurocognitive performance was not significantly worse among amyloid-positive compared with amyloid-negative participants. Amyloid deposition can be identified among cognitively normal elderly persons during life, and the prevalence of asymptomatic amyloid deposition may be similar to that of symptomatic amyloid deposition. In this group of participants without clinically significant impairment, amyloid deposition was not associated with worse cognitive function, suggesting that an elderly person with a significant amyloid burden can remain cognitively normal. However, this finding is based on relatively small numbers and needs to be replicated in larger cohorts. Longitudinal follow-up of these subjects will be required to support the potential of PiB imaging to identify preclinical Alzheimer disease, or, alternatively, to show that amyloid deposition is not sufficient to cause Alzheimer disease within some specified period.
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            The association between quantitative measures of dementia and of senile change in the cerebral grey matter of elderly subjects.

            G Blessed, B. Tomlinson, M. Roth (1968)
            Article 0 comments Cited 119 times – based on 0 reviews     Review now
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              Exome sequencing of ion channel genes reveals complex profiles confounding personal risk assessment in epilepsy.

              Tara Leah Klassen, Caleb Davis, Alica Goldman … (2011)
              Ion channel mutations are an important cause of rare Mendelian disorders affecting brain, heart, and other tissues. We performed parallel exome sequencing of 237 channel genes in a well-characterized human sample, comparing variant profiles of unaffected individuals to those with the most common neuronal excitability disorder, sporadic idiopathic epilepsy. Rare missense variation in known Mendelian disease genes is prevalent in both groups at similar complexity, revealing that even deleterious ion channel mutations confer uncertain risk to an individual depending on the other variants with which they are combined. Our findings indicate that variant discovery via large scale sequencing efforts is only a first step in illuminating the complex allelic architecture underlying personal disease risk. We propose that in silico modeling of channel variation in realistic cell and network models will be crucial to future strategies assessing mutation profile pathogenicity and drug response in individuals with a broad spectrum of excitability disorders. Copyright © 2011 Elsevier Inc. All rights reserved.
              Article 0 comments Cited 96 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 9502015
                Journal ID (pubmed-jr-id): 8791
                Journal ID (nlm-ta): Nat Med
                Journal ID (iso-abbrev): Nat. Med.
                Title: Nature medicine
                ISSN (Print): 1078-8956
                ISSN (Electronic): 1546-170X
                Publication date Nihms-submitted: 21 March 2017
                Publication date (Electronic): 01 May 2017
                Publication date (Print): June 2017
                Publication date PMC-release: 01 November 2017
                Volume: 23
                Issue: 6
                Pages: 678-680
                Affiliations
                [1 ]MGH Epilepsy Service, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA
                [2 ]Department of Neurology, Baylor College of Medicine, Houston, Texas, USA
                [3 ]Department of Neurosurgery, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA
                Author notes
                Address for Correspondence: Andrew J. Cole, M.D., Director, MGH Epilepsy Service, Professor of Neurology, Harvard Medical School, Massachusetts General Hospital, Wang ACC 739 L, Fruit Street, Boston, Massachusetts 02114, Tel: 617 726-3311, Fax: 617 726-9207, cole.andrew@ 123456mgh.harvard.edu
                Article
                Manuscript ID: NIHMS861286
                DOI: 10.1038/nm.4330
                PMC ID: 5461182
                PubMed ID: 28459436
                SO-VID: 72efc45a-cc7f-41fe-928b-2706593b1150
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                Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

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                ScienceOpen disciplines: Medicine

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