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Review
. 2017 Apr;18(3):162-214.
doi: 10.1080/15622975.2016.1190867. Epub 2016 Jul 15.

Biological markers for anxiety disorders, OCD and PTSD: A consensus statement. Part II: Neurochemistry, neurophysiology and neurocognition

Borwin Bandelow  1 , David Baldwin  2 , Marianna Abelli  3 , Blanca Bolea-Alamanac  4 , Michel Bourin  5 , Samuel R Chamberlain  6   7 , Eduardo Cinosi  8 , Simon Davies  9   4 , Katharina Domschke  10 , Naomi Fineberg  6 , Edna Grünblatt  10   11   12   13 , Marek Jarema  14 , Yong-Ku Kim  15 , Eduard Maron  16   17   18 , Vasileios Masdrakis  19 , Olya Mikova  20 , David Nutt  18 , Stefano Pallanti  21 , Stefano Pini  3 , Andreas Ströhle  22 , Florence Thibaut  23 , Matilde M Vaghi  24 , Eunsoo Won  15 , Dirk Wedekind  1 , Adam Wichniak  14 , Jade Woolley  2 , Peter Zwanzger  25   26 , Peter Riederer  10
Affiliations
Review

Biological markers for anxiety disorders, OCD and PTSD: A consensus statement. Part II: Neurochemistry, neurophysiology and neurocognition

Borwin Bandelow et al. World J Biol Psychiatry. 2017 Apr.

Abstract

Objective: Biomarkers are defined as anatomical, biochemical or physiological traits that are specific to certain disorders or syndromes. The objective of this paper is to summarise the current knowledge of biomarkers for anxiety disorders, obsessive-compulsive disorder (OCD) and posttraumatic stress disorder (PTSD).

Methods: Findings in biomarker research were reviewed by a task force of international experts in the field, consisting of members of the World Federation of Societies for Biological Psychiatry Task Force on Biological Markers and of the European College of Neuropsychopharmacology Anxiety Disorders Research Network.

Results: The present article (Part II) summarises findings on potential biomarkers in neurochemistry (neurotransmitters such as serotonin, norepinephrine, dopamine or GABA, neuropeptides such as cholecystokinin, neurokinins, atrial natriuretic peptide, or oxytocin, the HPA axis, neurotrophic factors such as NGF and BDNF, immunology and CO2 hypersensitivity), neurophysiology (EEG, heart rate variability) and neurocognition. The accompanying paper (Part I) focuses on neuroimaging and genetics.

Conclusions: Although at present, none of the putative biomarkers is sufficient and specific as a diagnostic tool, an abundance of high quality research has accumulated that should improve our understanding of the neurobiological causes of anxiety disorders, OCD and PTSD.

Keywords: Anxiety disorders; genetic; neurobiology; neurochemistry; neuroimaging; review.

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Conflict of interest statement

All other authors reported no conflicts of interest to declare.

Figures

Figure 1
Figure 1
GABA-A receptor and subunit structure; GABA and benzodiazepine (BZD) binding site (Domschke & Zwanzger 2008).
Figure 2
Figure 2
Stress-induced interactions between nervous, endocrine and immune systems. The hypothalamus secretes CRH in response to stress, and from the paraventricular nucleus of the hypothalamus. CRH-containing neurons have projections to the locus coeruleus. The locus coeruleus sends direct projections to the sympathetic and parasympathetic preganglionic neurons, increasing sympathetic activity and decreasing parasympathetic activity through the activation of adrenoceptors. In turn, the activation of the sympathetic nervous system stimulates the release of CRH. The products of sympathetic and parasympathetic nervous system activity are NE and E, and ACh, respectively. When stress is prolonged, as in anxiety disorders, the sympathetic nervous system continues to be activated with a lack of parasympathetic counteractivity. As a result, NE and E levels are increased and ACh levels are decreased, which leads to an increased release of pro-inflammatory cytokines from immune cells. Pro-inflammatory cytokines such as TNF, IL1 and IL6 then trigger the activation of the sympathetic nervous system. CRH, corticotropin-releasing hormone; NE, norepinephrine; E, epinephrine; ACh, acetylcholine, TNF, tumour necrosis factor; IL1, interleukin-1; IL6, interleukin-6; +, stimulation; −, inhibition.
See this image and copyright information in PMC

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