The long-term goal of this project is to develop a comprehensive set of standardized Amyotrophic Lateral Sclerosis (ALS) clinical predictors that can be used to successfully characterize, diagnose, prognose, manage, and treat this devastating neurodegenerative disease. Specifically, the goal of this proposal is to identify and prioritize potential clinical predictors by exploring the relationships among measures and data recorded in retrospective ALS clinic patient records.
The specific aims of this proposal are to: 1) Construct a multi-variate relational ALS patient database that organizes and translates raw records, both on a patient and per-visit basis, into unified structures required for data mining analyses;2) Assess correlations of ALS patient clinic measures using standard parametric/non-parametric analyses as well as novel, dynamic relational analyses capable of revealing temporal changes/patterns with disease progression. The primary outcomes of this R21 proposal are a prioritized list of promising ALS clinical predictors and the developed plans by which to pursue them in future in-depth statistical studies. The secondary outcome is one of the largest, detailed, and all- inclusive data sets on clinical ALS.

Public Health Relevance

This project is highly relevant to public health as it seeks to identify demographic, onset, prognostic, and treatment clinical predictors that aid clinicians in the management and intervention of the neurodegenerative disease Amyotrophic Lateral Sclerosis (ALS).

Agency
National Institute of Health (NIH)
Type
Exploratory/Developmental Grants (R21)
Project #
5R21NS081426-02
Application #
8657124
Study Section
Clinical Neuroscience and Neurodegeneration Study Section (CNN)
Program Officer
Gubitz, Amelie
Project Start
Project End
Budget Start
Budget End
Support Year
2
Fiscal Year
2014
Total Cost
Indirect Cost
Name
Georgia Institute of Technology
Department
Engineering (All Types)
Type
Biomed Engr/Col Engr/Engr Sta
DUNS #
City
Atlanta
State
GA
Country
United States
Zip Code
30332
Hollinger, Sabrina K; Okosun, Ike S; Mitchell, Cassie S (2016) Antecedent Disease and Amyotrophic Lateral Sclerosis: What Is Protecting Whom? Front Neurol 7:47
Foley, Avery M; Ammar, Zeena M; Lee, Robert H et al. (2015) Systematic review of the relationship between amyloid-β levels and measures of transgenic mouse cognitive deficit in Alzheimer's disease. J Alzheimers Dis 44:787-95
Irvin, Cameron W; Kim, Renaid B; Mitchell, Cassie S (2015) Seeking homeostasis: temporal trends in respiration, oxidation, and calcium in SOD1 G93A Amyotrophic Lateral Sclerosis mice. Front Cell Neurosci 9:248
Jeyachandran, Amilia; Mertens, Benjamin; McKissick, Eric A et al. (2015) Type I Vs. Type II Cytokine Levels as a Function of SOD1 G93A Mouse Amyotrophic Lateral Sclerosis Disease Progression. Front Cell Neurosci 9:462
Lee, Robert H; Mitchell, Cassie S (2015) Axonal transport cargo motor count versus average transport velocity: is fast versus slow transport really single versus multiple motor transport? J Theor Biol 370:39-44
Kim, Renaid B; Irvin, Cameron W; Tilva, Keval R et al. (2015) State of the field: An informatics-based systematic review of the SOD1-G93A amyotrophic lateral sclerosis transgenic mouse model. Amyotroph Lateral Scler Frontotemporal Degener 17:1-14
Coan, Grant; Mitchell, Cassie S (2015) An Assessment of Possible Neuropathology and Clinical Relationships in 46 Sporadic Amyotrophic Lateral Sclerosis Patient Autopsies. Neurodegener Dis 15:301-12
Mitchell, Cassie S; Cates, Ashlyn; Kim, Renaid B et al. (2015) Undergraduate Biocuration: Developing Tomorrow's Researchers While Mining Today's Data. J Undergrad Neurosci Educ 14:A56-65
Mitchell, Cassie S; Hollinger, Sabrina K; Goswami, Shivani D et al. (2015) Antecedent Disease is Less Prevalent in Amyotrophic Lateral Sclerosis. Neurodegener Dis 15:109-13
Pfohl, Stephen R; Halicek, Martin T; Mitchell, Cassie S (2015) Characterization of the Contribution of Genetic Background and Gender to Disease Progression in the SOD1 G93A Mouse Model of Amyotrophic Lateral Sclerosis: A Meta-Analysis. J Neuromuscul Dis 2:137-150