SPECIAL SESSIONS
340
PLENARY LECTURE
sat, 29 nov 2014 | 12.00 – 13.00 h | hall a6
D
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The future of depression treatment
Florian Holsboer, Munich (Germany)
Chairs:
Peter Falkai, Munich (Germany)
Frank Schneider, Aachen (Germany)
We can thank the skills and intuition of the Swiss psychiatrists Roland Kuhn and Jules Angst
for the discovery of antidepressants. Intensive research for over half a century has resulted
in improvements in side effects but not in clinical efficacy. There are many reasons for the
developmental standstill, but the most important are as follows:
1. The concept “from bench to bed” has not resulted in new therapies and was maintained
for too long.
2. There are no animal models for depression; conventional animal models have no predic-
tive validity for the efficacy of new candidate antidepressants.
3. The transition from animal research to human studies happens too late.
4. Academic research does not make enough use of the possibilities of chemical biology to
generate new, innovative candidate drugs.
5. New drugs with specific effects against depression are tested in controlled studies as if
they may have similar effects to conventional, nonspecific antidepressants. Stratifica-
tion on the basis of gene tests and biomarkers has not yet entered efficacy testing. This
results in negative study results, with the consequence that industrial research and the
development of new antidepressants are discontinued.
6. The interfaces between clinical and basic research, the pharmaceutical industry, sponsors
and the framework political conditions do not function well and rather inhibit innovation.
Future improvements in depression treatment require a departure from the “standard anti-
depressant” and the establishment of personalised therapy, based on the patient’s individ-
ual biosignature: this consists of laboratory data and includes genetics findings and con-
dition-related biomarkers, such as measurements of gene activity, quantitative proteomics
and metabolomics, together with complex data from EEG measurements, neuroendocrinol-
ogy and imaging.
In this way the mechanisms causing an illness can be matched with the clinical diagnosis
and drugs with a specific action can be used for targeted interventions.
This concept for the future will be demonstrated with the example of CRHR1 antagonists,
V1BR antagonists and the ABCB1 brain barrier test. The first successes in personalised de-
pression therapy can be expected from these projects.
