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Author Notes:

Correspondence to Cassie Mitchell, Senior Research Faculty, Department of Biomedical Engineering, Georgia Institute of Technology, 313 First Drive, Atlanta, Georgia, USA. E-mail: cassie.mitchell@bme.gatech.edu

The authors declare no conflict of interest with this manuscript.

Subjects:

Research Funding:

Grants were received from the USA National Institute of Health (NS081426 and NS069616) to CSM.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Clinical Neurology
  • Neurosciences & Neurology
  • Mitochondria
  • excitotoxicity
  • gliosis
  • protein aggregation
  • reactive oxygen species
  • rotarod
  • calcium
  • neuropathology
  • CU/ZN-SUPEROXIDE-DISMUTASE
  • MOTOR-NEURON DISEASE
  • LINKED SOD1 MUTANTS
  • AXONAL-TRANSPORT
  • OXIDATIVE STRESS
  • SPINAL MOTONEURONS
  • FAMILIAL ALS
  • THERAPEUTIC TARGET
  • SIGNALING PATHWAY
  • GLUTAMATE RELEASE

State of the field: An informatics-based systematic review of the SOD1-G93A amyotrophic lateral sclerosis transgenic mouse model

Tools:

Journal Title:

Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration

Volume:

Volume 17, Number 1-2

Publisher:

, Pages 1-14

Type of Work:

Article | Final Publisher PDF

Abstract:

Numerous sub-cellular through system-level disturbances have been identified in over 1300 articles examining the superoxide dismutase-1 guanine 93 to alanine (SOD1-G93A) transgenic mouse amyotrophic lateral sclerosis (ALS) pathophysiology. Manual assessment of such a broad literature base is daunting. We performed a comprehensive informatics-based systematic review or field analysis to agnostically compute and map the current state of the field. Text mining of recaptured articles was used to quantify published data topic breadth and frequency. We constructed a nine-category pathophysiological function-based ontology to systematically organize and quantify the field's primary data. Results demonstrated that the distribution of primary research belonging to each category is: systemic measures an motor function, 59%; inflammation, 46%; cellular energetics, 37%; proteomics, 31%; neural excitability, 22%; apoptosis, 20%; oxidative stress, 18%; aberrant cellular chemistry, 14%; axonal transport, 10%. We constructed a SOD1-G93A field map that visually illustrates and categorizes the 85% most frequently assessed sub-topics. Finally, we present the literature-cited significance of frequently published terms and uncover thinly investigated areas. In conclusion, most articles individually examine at least two categories, which is indicative of the numerous underlying pathophysiological interrelationships. An essential future path is examination of cross-category pathophysiological interrelationships and their co-correspondence to homeostatic regulation and disease progression.

Copyright information:

© 2015 Informa Healthcare

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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