Education & Outreach

Q&A: Hippocampal tail volume as a predictive biomarker of antidepressant treatment

After reading the lay summary on CAN-BIND paper entitled “Hippocampal Tail Volume as a Predictive Biomarker of Antidepressant Treatment”, we invited our community advisory committee members to share questions they had on the study. Below are some of these questions posed and answers by the first author of the paper, Dr. Nikita Nogovitsyn. Reviewed by Wegdan Abdelmoemin, Sagar Parikh and Andrew Kcomt.

Q: Why was the hippocampal tail specifically being measured as opposed to the whole hippocampus or another part of it?

A: Previous research showed that only posterior hippocampal parts are associated with clinical outcomes following antidepressant treatment. This is the rationale for our exclusive interest in a specific part of the hippocampus (MacQueen et al. 2008, Maller et al. 2018.)

Q: Why was escitalopram specifically used?  How do they differ?  I think some brief background information on the medications would offer helpful insight.

A: The Canadian Network for Mood and Anxiety Treatments (CANMAT) is an organization that provides clinical recommendations and treatment guideline for doctors. CANMAT guidelines indicate that a particular class of antidepressants, the selective serotonin reuptake inhibitors (SSRIs), should be the first-line option in the choice of treatment of depression. This decision was based on a number of clinical factors (e.g. safety, cost, patients ability to tolerate adverse drug effects). Among various types of SSRI’s, escitalopram has been shown to have some meaningful advantages over other medicaments of this class.

Q: Are there any conclusions why early remitters showed no volume disproportions or asymmetry?

A: There are many biological factors that may have influenced the degree of hippocampal disproportions in depressed patients. This is a very interesting research question, but one that we were unable to ascertain in our present paper.

Q: Is hippocampal atrophy an inborn thing predisposing to depression or as a result of the depression process itself? And how could we differentiate?

A: Converging lines of evidence now support the notion that hippocampal atrophy can be sequelae of a significant history of depression and an inborn biological deviation. Perhaps, future studies may attempt to differentiate between these phenomena.

Q: Are there any implications for psychotherapy treatments for depression or any ideas the authors have about how hippocampal volume might impact the effectiveness of talk therapies, or the use of talk therapies together with medication?

A: While psychotherapy is a well-recognized strategy for treating depression, the CAN-BIND-1 was primarily designed with a focus on pharmacotherapy.