A Framework for the Assessment of Surrogate Models of Psychiatric Disorders: Attention-Deficit/Hyperactivity Disorder A Case Study
This thesis examines the efficacy of rodent models for the understanding and treatment of Attention-Deficit/Hyperactivity Disorder (AD/HD). A key tool used within biomedicine are ‘surrogate model’s, which aim to represent a human target system. One area of research using surrogate models is dedicated to researching the aetiology and treatment for AD/HD. There are over 20 distinct rodent models for studying AD/HD; however, the efficacy of these models, as well as surrogate models in general, is a subject of ongoing debate due to limited translation rates from animal studies to human applications. This debate is particularly pronounced in psychiatric disorders like AD/HD, which involve complicated socio-cultural and environmental factors that are challenging to replicate in laboratory settings. This thesis evaluates surrogate models in biomedicine, specifically rodents, by examining their historical development, justifications, and problematic assumptions. To understand how to critique surrogate models, a framework is developed based on common criticisms of surrogate models to assess research validity. I apply the framework to six studies assessing rodents' aetiology and treatment of AD/HD. The six studies reveal limitations in rodent models' ability to capture the construct of AD/HD fully. The sample of studies did not satisfy the requirements for mechanistic explanation set out in this thesis, indicating an area for further refinement. The exploratory function of the models used in the six studies and inconsistent epistemic context compound unknown variables and increase the risk of false positives and negatives. Inconsistent rodent handling and tests of the human AD/HD construct contradict the tenant of such models' uniformity. Finally, the lack of reference to the relevant diagnostic criteria in assessing AD/HD in surrogate models challenges how much the research’s constructs and findings can be associated with human AD/HD.