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      Taurine in drinking water recovers learning and memory in the adult APP/PS1 mouse model of Alzheimer's disease

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          Abstract

          Alzheimer's disease (AD) is a lethal progressive neurological disorder affecting the memory. Recently, US Food and Drug Administration mitigated the standard for drug approval, allowing symptomatic drugs that only improve cognitive deficits to be allowed to accelerate on to clinical trials. Our study focuses on taurine, an endogenous amino acid found in high concentrations in humans. It has demonstrated neuroprotective properties against many forms of dementia. In this study, we assessed cognitively enhancing property of taurine in transgenic mouse model of AD. We orally administered taurine via drinking water to adult APP/PS1 transgenic mouse model for 6 weeks. Taurine treatment rescued cognitive deficits in APP/PS1 mice up to the age-matching wild-type mice in Y-maze and passive avoidance tests without modifying the behaviours of cognitively normal mice. In the cortex of APP/PS1 mice, taurine slightly decreased insoluble fraction of Aβ. While the exact mechanism of taurine in AD has not yet been ascertained, our results suggest that taurine can aid cognitive impairment and may inhibit Aβ-related damages.

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          Co-expression of multiple transgenes in mouse CNS: a comparison of strategies.

          Joanna Jankowsky, Hilda H Slunt, Tamara Ratovitski … (2001)
          The introduction of two transgenes into one animal is increasingly common as transgenic experiments become more sophisticated. In this study we examine two strategies for creating double transgenic founders from a single microinjection. In the first approach, two constructs, each with its own promoter element, were coinjected into the pronucleus. In the second approach, both transgenes were cloned into one vector, separated by an internal ribosomal entry site (IRES), and placed under control of a single promoter. Both strategies save time and increase the percentage of double transgenic offspring over the standard method of mating single transgenic lines. However, despite high transgene copy numbers, the bicistronic lines did not show robust expression of either protein. Copy number and protein expression correlated much better in the coinjected lines, with expression levels in one line approaching that observed in some of our best single transgenic controls. Thus we recommend coinjection of individual plasmids for the generation of multiply transgenic founders.
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            Sp1 and TAFII130 transcriptional activity disrupted in early Huntington's disease.

            David G. Standaert, Douglas Young, Naoko Tanese … (2002)
            Huntington's disease (HD) is an inherited neurodegenerative disease caused by expansion of a polyglutamine tract in the huntingtin protein. Transcriptional dysregulation has been implicated in HD pathogenesis. Here, we report that huntingtin interacts with the transcriptional activator Sp1 and coactivator TAFII130. Coexpression of Sp1 and TAFII130 in cultured striatal cells from wild-type and HD transgenic mice reverses the transcriptional inhibition of the dopamine D2 receptor gene caused by mutant huntingtin, as well as protects neurons from huntingtin-induced cellular toxicity. Furthermore, soluble mutant huntingtin inhibits Sp1 binding to DNA in postmortem brain tissues of both presymptomatic and affected HD patients. Understanding these early molecular events in HD may provide an opportunity to interfere with the effects of mutant huntingtin before the development of disease symptoms.
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              β-Amyloid burden in healthy aging: regional distribution and cognitive consequences.

              K Rodrigue, K Kennedy, M D Devous … (2012)
              Several lines of evidence suggest that pathologic changes underlying Alzheimer disease (AD) begin years prior to the clinical expression of the disease, underscoring the need for studies of cognitively healthy adults to capture these early changes. The overall goal of the current study was to map the cortical distribution of β-amyloid (Aβ) in a healthy adult lifespan sample (aged 30-89), and to assess the relationship between elevated amyloid and cognitive performance across multiple domains. A total of 137 well-screened and cognitively normal adults underwent Aβ PET imaging with radiotracer (18)F-florbetapir. Aβ load was estimated from 8 cortical regions. Participants were genotyped for APOE and tested for processing speed, working memory, fluid reasoning, episodic memory, and verbal ability. Aβ deposition is distributed differentially across the cortex and progresses at varying rates with age across cortical brain regions. A subset of cognitively normal adults aged 60 and over show markedly elevated deposition, and also had a higher rate of APOE ε4 (38%) than nonelevated adults (19%). Aβ burden was linked to poorer cognitive performance on measures of processing speed, working memory, and reasoning. Even in a highly selected lifespan sample of adults, Aβ deposition is apparent in some adults and is influenced by APOE status. Greater amyloid burden was related to deleterious effects on cognition, suggesting that subtle cognitive changes accrue as amyloid progresses.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 12 December 2014
                Publication date Collection: 2014
                Volume: 4
                Electronic Location Identifier: 7467
                Affiliations
                [1 ]Center for Neuro-Medicine, Brain Science Institute, Korea Institute of Science and Technology , Seoul, Republic of Korea
                [2 ]Biological Chemistry Program, Korea University of Science and Technology , Daejeon, Republic of Korea
                [3 ]Department of Biochemistry and Biomedical Sciences, Seoul National University, College of Medicine , Seoul, Republic of Korea
                [4 ]Department of Biology, Massachusetts Institute of Technology , Cambridge, MA, U.S.A.
                [5 ]Department of Applied Chemistry, Dongduk Women's University , Seoul, Republic of Korea
                [6 ]Center for Neuroscience, Brain Science Institute, Korea Institute of Science and Technology , Seoul, Republic of Korea
                Author notes
                [*]

                These authors contributed equally to this work.

                Article
                Publisher Item ID: srep07467
                DOI: 10.1038/srep07467
                PMC ID: 4264000
                PubMed ID: 25502280
                SO-VID: 27cfbb7c-51dc-4f00-b79f-48b79a5eb1b4
                Copyright © Copyright © 2014, Macmillan Publishers Limited. All rights reserved
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder in order to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/

                History
                Date received : 02 September 2014
                Date accepted : 25 November 2014
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