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SPECIAL TOPICS

Multiple Sclerosis

Published: September 2008
 

The baseline time span for this database is (publication years) 1998-April 30, 2008 from the second bimonthly update (a 10-year + 4-month period). The resulting database contained 7,808 (10 years) and 2,185 (2 years) papers; 17,918 authors; 81 nations; 918 journals; and 4,673 institutions.

Top 20 Papers

  10-year period
  2-year period

Top 20 Overall

  Authors
  Institutions
  Journals
  Nations

Research Front Map

  Map title: "Multiple Sclerosis"

Time Series

  1- & 5-year periods

Field Distribution

Interviews

  Interviews, first-person essays, and profiles about people in a wide variety of fields which pertain to this special topic of Multiple Sclerosis.
   

OVERVIEW

Multiple sclerosis (MS) is a chronic, inflammatory disease of the central nervous system in which the body's own immune system attacks the myelin sheath that protects the nerve fibers. According to the National Multiple Sclerosis Society, MS affects approximately 2.5 million people worldwide, with 400,000 of these cases in the US, and 200 new cases diagnosed every week. This month, ScienceWatch.com examines the literature on MS over the past decade and over the past two years.

The emerging themes in MS research from over the past decade include the pathogenesis of lesions, the role of autoantibodies in myelin damage, axonal transaction, and gene microarray analysis of the lesions themselves. Other potential players in the development or progress of MS, such as chemokines, chemokine receptors, and regulatory T cells, are also discussed. Treatments studied include interferon beta 1-a, interferon beta 1-b, natalizumab, and stem cells. Diagnostic criteria and the increasingly helpful role of MRI in understanding the disease are also addressed.

Several of the topics on the 10-year list are still prevalent in more recent research, including the role of chemokines in the pathogenesis of MS, and treatment with interferons beta 1-a and 1-b. Other drug trials look at the combination of natalizumab and interferon beta 1-a, fingolimod (FTY720), and glatiramer acetate. The value of animal models of experimental allergic encephalomyelitis in understanding MS, genome studies of risk alleles, the relation of MS to Epstein-Barr virus, the occurrence of remyelination in certain patients, the cause of axonal degeneration, and the optimal window of opportunity for treatment are also topics of interest in the past two years..

Methodology: To construct this database, papers were extracted for the special topic of Multiple Sclerosis based this search criteria:

Title=("multiple sclerosis")
Refined by: Document Type=(ARTICLE OR REVIEW)

The baseline time span for this database is (publication years) 1998-April 30, 2008 from the second bimonthly update (a 10-year + 4-month period). The resulting database contained 7,808 (10 years) and 2,185 (2 years) papers; 17,918 authors; 81 nations; 918 journals; and 4,673 institutions.

Rankings: Once the database was in place, it was used to generate the lists of top 20 papers (two- and ten-year periods), authors, journals, institutions, and nations, covering a time span of 1998-April 30, 2008 (second bimonthly period 2008).

The top 20 papers are ranked according to total cites. Rankings for author, journal, institution, and country are listed in three ways: according to total cites, total papers, and total cites/paper. The paper thresholds and corresponding percentages used to determine scientist, institution, country, and journal rankings according to total cites/paper, and total papers respectively are as follows:

Entity Authors Institutions Nations Journals
Thresholds 33 93 16 2
Percentage: 1% 1% 50% 50%

Special Topic Keywords: multiple sclerosis, relapsing-remitting multiple sclerosis, brain lesions, pathogenesis, demyelination, central nervous system, chemokines, interferon beta-1a, T cells, natalizumab, neurospheres, interferon beta-1b, MRI, fingolimod, mitochondrial dysfunction, animal models, remyelination, risk alleles, immune surveillance, visual function, neurobiology, neurodegeneration, glatiramer acetate.



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