Animal models of autogenous/reactive subtyped obsessive-compulsive disorder

Keywords: cognition inhibition; obsessive-compulsive disorder; response inhibition

Note: Linked articles are emboldened. This informal proposal is meant for illustrating my research interests only.

Cognition inhibition deficits serve as a cognitive biomarker for the autogenous subtype of the obsessive-compulsive disorder (OCD), with regard to the reactive subtype (Fan et al., 2016; in the article, interference control is an alias for cognition inhibition). While the reactive subtype is characterized by impairments in response inhibition but not cognition inhibition, the autogenous subtype features both.

In a recent study, Fan et al. further investigated this heterogeneity by looking at the functional connectivity profiles of both subtypes. Specifically, weaker within-network connectivity in proposed cognition inhibition networks based on previous research was found in OCD patients with the autogenous subtype.

It seems that previous research using animal models did not differentiate much between the autogenous/reactive subtypes and used behaviors such as excessive self-grooming as representation of OCD. These confrontational compulsions can be characterized as more related to the reactive-type OCD. A frequent external manifestation of autogenous-type OCD is maladaptive avoidance. The practice of measuring maladaptive avoidance in animals appears less seen for the purpose of OCD research, nevertheless, well documented in the literature. I suggest using behaviors such as self-grooming and avoidant behaviors to represent specific OCD subtypes in animal models.

I suggest an attempt to test the hypothesis that animal models (presumably, rodents) with experimentally depressed activity and connectivity levels in networks related to cognition inhibition (not overlapping with that related to response inhibition) will exhibit autogenous-type OCD related compulsions more frequently, compared to controls. Supression of activity and connectivity may be realized through knock-down mutants, optogenetics, etc. The specific design of experimental control may come in many forms, for example: comparing with the group having deficits in both cognition inhibition and response inhibition related networks and with the group having other combinations of deficits.