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Analysis of institutional authors

Sola Subirana, CarmenOthersComella Bolla AAuthorValente TAuthorMiguez AAuthorBrito VAuthorGines SAuthorStraccia MCorresponding AuthorCanals JmCorresponding Author

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December 3, 2019
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Article

CD200 is up-regulated in R6/1 transgenic mouse model of Huntington's disease

Publicated to: PLoS One. 14 (12): e0224901- - 2019-12-02 14(12), DOI: 10.1371/journal.pone.0224901

Authors:

Bolla, AC; Valente, T; Miguez, A; Brito, V; Gines, S; Sol, C; Straccia, M; Canals, JM
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Affiliations

August Pi & Sunyer Biomed Res Inst IDIBAPS, Barcelona, Spain - Author
Consejo Super Invest Cient & IBB CSIC, Dept Cerebral Ischem & Neurodegenerat, Inst Invest Biomed Barcelona, Barcelona, Spain - Author
FRESCI, Barcelona, Spain - Author
Network Ctr Biomed Res Neurodegenerat Dis CIBERNE, Madrid, Spain - Author
Univ Barcelona, Fac Med & Hlth Sci, Dept Biomed, Barcelona, Spain - Author
Univ Barcelona, Neurosci Inst, Barcelona, Spain - Author
Univ Barcelona, Stem Cells & Regenerat Med Lab, Prod & Validat Ctr Adv Therapies Creatio, Dept Biomed,Fac Med & Hlth Sci, Barcelona, Spain - Author
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Abstract

In Huntington's disease (HD), striatal medium spiny neurons (MSNs) are particularly sensitive to the presence of a CAG repeat in the huntingtin (HTT) gene. However, there are many evidences that cells from the peripheral immune system and central nervous system (CNS) immune cells, namely microglia, play an important role in the etiology and the progression of HD. However, it remains unclear whether MSNs neurodegeneration is mediated by a non-cell autonomous mechanism. The homeostasis in the healthy CNS is maintained by several mechanisms of interaction between all brain cells. Neurons can control microglia activation through several inhibitory mechanisms, such as the CD200-CD200R1 interaction. Due to the complete lack of knowledge about the CD200-CD200R1 system in HD, we determined the temporal patterns of CD200 and CD200R1 expression in the neocortex, hippocampus and striatum in the HD mouse models R6/1 and HdhQ111/7 from pre-symptomatic to manifest stages. In order to explore any alteration in the peripheral immune system, we also studied the levels of expression of CD200 and CD200R1 in whole blood. Although CD200R1 expression was not altered, we observed and increase in CD200 gene expression and protein levels in the brain parenchyma of all the regions we examined, along with HD pathogenesis in R6/1 mice. Interestingly, the expression of CD200 mRNA was also up-regulated in blood following a similar temporal pattern. These results suggest that canonical neuronal-microglial communication through CD200-CD200R1 interaction is not compromised, and CD200 up-regulation in R6/1 brain parenchyma could represent a neurotrophic signal to sustain or extend neuronal function in the latest stages of HD as pro-survival mechanism.
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Keywords

cag repeatcd200-deficient miceexpressionhippocampusimmune activationinhibitory moleculesmicroglial activationneuroinflammationreceptorCag repeatCd200-deficient miceCorea de huntingtonExpressionHippocampusHuntington's choreaImmune activationInduced cognitive impairmentInhibitory moleculesMicroglial activationNeuroinflammationReceptor

Quality index

Bibliometric impact. Analysis of the contribution and dissemination channel

The work has been published in the journal PLoS One due to its progression and the good impact it has achieved in recent years, according to the agency Scopus (SJR), it has become a reference in its field. In the year of publication of the work, 2019, it was in position , thus managing to position itself as a Q1 (Primer Cuartil), in the category Multidisciplinary. Notably, the journal is positioned above the 90th percentile.

Independientemente del impacto esperado determinado por el canal de difusión, es importante destacar el impacto real observado de la propia aportación.

Según las diferentes agencias de indexación, el número de citas acumuladas por esta publicación hasta la fecha 2026-04-06:

  • WoS: 9
  • Scopus: 8
  • Europe PMC: 5
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Impact and social visibility

From the perspective of influence or social adoption, and based on metrics associated with mentions and interactions provided by agencies specializing in calculating the so-called "Alternative or Social Metrics," we can highlight as of 2026-04-06:

  • The use, from an academic perspective evidenced by the Altmetric agency indicator referring to aggregations made by the personal bibliographic manager Mendeley, gives us a total of: 29.
  • The use of this contribution in bookmarks, code forks, additions to favorite lists for recurrent reading, as well as general views, indicates that someone is using the publication as a basis for their current work. This may be a notable indicator of future more formal and academic citations. This claim is supported by the result of the "Capture" indicator, which yields a total of: 29 (PlumX).

With a more dissemination-oriented intent and targeting more general audiences, we can observe other more global scores such as:

  • The Total Score from Altmetric: 13.
  • The number of mentions on the social network X (formerly Twitter): 5 (Altmetric).
  • The number of mentions in news outlets: 1 (Altmetric).

It is essential to present evidence supporting full alignment with institutional principles and guidelines on Open Science and the Conservation and Dissemination of Intellectual Heritage. A clear example of this is:

  • The work has been submitted to a journal whose editorial policy allows open Open Access publication.
  • Assignment of a Handle/URN as an identifier within the deposit in the Institutional Repository: http://hdl.handle.net/10261/205174
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Leadership analysis of institutional authors

There is a significant leadership presence as some of the institution’s authors appear as the first or last signer, detailed as follows: First Author (Comella Bolla, Andrea) and Last Author (Canals Coll, Josep M).

the authors responsible for correspondence tasks have been Straccia, Marco and Canals Coll, Josep M.

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Project objectives

Los objetivos perseguidos en esta aportación se centran en profundizar en el papel del sistema CD200-CD200R1 en la enfermedad de Huntington (HD). Se pretende determinar los patrones temporales de expresión de CD200 y CD200R1 en neocórtex, hipocampo y cuerpo estriado en modelos murinos R6/1 y HdhQ111/7 desde etapas pre-sintomáticas hasta manifestadas. Además, se busca analizar las alteraciones en el sistema inmunitario periférico mediante la evaluación de la expresión de CD200 y CD200R1 en sangre total. También se aspira a caracterizar la relación entre la expresión de CD200 y la patogénesis de HD en R6/1. Finalmente, se pretende evaluar si la comunicación neuronal-microglial a través de CD200-CD200R1 se mantiene intacta y su posible función neurotrófica en etapas avanzadas de la enfermedad.
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Most relevant results

El estudio analiza la expresión de CD200 y CD200R1 en modelos murinos de Huntington (R6/1 y HdhQ111/7) desde etapas pre-sintomáticas hasta manifestaciones clínicas. Se observaron los siguientes resultados relevantes: 1) La expresión de CD200R1 no mostró alteraciones significativas en las regiones cerebrales estudiadas. 2) Se detectó un aumento en la expresión génica y niveles proteicos de CD200 en el parénquima cerebral de neocórtex, hipocampo y cuerpo estriado en ratones R6/1 durante la progresión de la enfermedad. 3) La expresión de ARNm de CD200 también se incrementó en sangre periférica siguiendo un patrón temporal similar. 4) Estos hallazgos indican que la comunicación neuronal-microglial mediada por CD200-CD200R1 no se ve comprometida en Huntington.
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Awards linked to the item

This study was supported by grants from the Ministerio de Ciencia, Innovacion y Universidades (Spain), (RTI2018-099001-B-I00 to JMC); Instituto de Salud Carlos III, Ministerio de Ciencia, Innovacion y Universidades and European Regional Development Fund (ERDF) [CIBERNED and RETICS (Red de Terapia Celular, RD16/0011/0012 to JMC)], Spain; Generalitat de Catalunya (2017SGR-1408 to J. M. C.), Spain; the CHDI Foundation (A12076 to JMC), USA; and ADVANCE (CAT) with the support of ACCIO (Catalonia Trade & Investment; Generalitat de Catalunya) and the European Community under the Catalonian ERDF operational program 2014-2020], Spain. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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