Barcelona snapshots

Prof. Gitte Moos Knudsen

Gitte Moos Knudsen psychiatrist Controversias Psiquiatry Barcelona
Københavns Universitet, Denmark
Talk Predictive biomarkers of treatment efficacy
Date Thursday, April 25th, 2019
Time 18:45 to 19:30
Round Table Generic aspects of resistance development


Gitte Moos Knudsen. Chief neurologist at Dept Neurology and chairman at the Neurobiology Research Unit (NRU), Rigshospitalet, and Director of Center for Experimental Medicine Neuropharmacology (NeuroPharm). Professor in Clinical Neurobiology at the University of Copenhagen (UCPH).

Appointments: Visiting scientist at NIH and at Stony Brook, USA (1985-90), and at MGH Harvard, Boston (2011-12). Clinical education has predominantly taken place at Rigshospitalet, interspersed by time as research fellow (1986-1989) and by maternal leave in 1989, 1992, and 1995. Research professor in Neurobiology and chief neurologist in 1999. Professor of Neurology at UCPH 2005-06 and of Neurobiology from 2004. Director of the Lundbeck Foundation Center for Integrated Molecular Brain Imaging - Cimbi (2006-15).

Research focus: I am a translational neurobiologist and clinical neurologist with interest in advanced methodological developments that I subsequently apply in my research to address pertinent neurobiological and clinical issues. I have a particular focus on multimodality neuroimaging of neuro-transmission in healthy individuals and in patients with neurological or psychiatric disorders.

Publications: Published 358 Medline indexed scientific papers and 28 books/book chapters.
No. citations >13,900. H-index: 58 (GoogleScholar).


There is currently an enormous unmet need for the development of effective precision medicine approaches for brain disorders. More precise treatment strategies are needed to replace the present “one-size-fits-all” and subsequent “trial-and error” approach currently applied in our patients. An important step to achieve this goal is to uncover endophenotypes and biomarkers that can critically help to stratify patient cohorts. To enable stratification of patients based on their underlying pathogenetic and pathophysiological brain disturbances will provide “enriched” patient populations that are more likely to benefit from specific interventions. Stratification will also be enormously beneficial for interpretation of clinical trials that aim to test new compounds and is essential to allow for an optimised treatment of patients with brain disorders. Another important challenge is to determine the target engagement of pharmacological interventions, and to predict occupancy based on, e.g., plasma drug concentrations.

A biomarker should be assessable objectively and provide information about physiological or pathological processes or responses to treatment interventions. Biomarkers should thus be able to help diagnose and stage a disorder, to give a prognostic outline or to predict treatment outcome. A biomarker is a measurable indicator of some biological state or condition and could be, e.g., tissue, blood or cerebrospinal fluid biochemistry, neuroimaging in terms of MRI (structural, spectroscopic, functional) or Positron Emission Tomography (PET), genomics, or EEG.

Biomarkers are often used to examine normal biological processes, pathogenic processes, or pharmacologic responses to an intervention; they can be prognostic or predictive. Whereas the prognostic biomarkers indicate the likelihood of patient outcome regardless of treatment then predictive biomarkers indicates the likelihood of a patient benefiting from a specific therapy. A focus on neuropharmacological interventions represents a highly relevant theme in precision medicine, to address the question of how we determine which patients best benefit from pharmacological treatments. The determination of specific patient features that predict drug response can potentially also have profound impact for the design of future drug trials.

The lecture will focus on biomarkers that have been proposed to be useful in mood disorders, both in terms of defining patients versus healthy controls, and for prediction of treatment efficacy.


[web] Madsen K et al (2015). Familial risk for major depression is associated with lower striatal 5-HT4 receptor binding. Int J Neuropsychopharmacol. 2015 Jan; 18(1): pyu034.

[PDF] McMahon B et al (2016). Seasonal difference in brain serotonin transporter binding predicts symptom severity in patients with seasonal affective disorder. Brain. 2016 May;139(Pt 5):1605-14. doi: 10.1093/brain/aww043. Epub 2016 Mar 19.

[PDF] Madsen K et al (2019). Psychedelic effects of psilocybin correlate with serotonin 2A receptor occupancy and plasma psilocin levels. Neuropsychopharmacology. 2019 Jan 26. doi: 10.1038/s41386-019-0324-9. [Epub ahead of print]