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

Bandelow, Borwin; Baldwin, David S.; Abelli, Marianna; Bolea-Alamañac, Blanca; Bourin, Michel; Chamberlain, Samuel R.; Cinosi, Eduardo; Davies, Simon; Domschke, Katharina; Fineberg, Naomi; Grünblatt, Edna; Jarema, Marek; Kim, Yong Ku; Maron, Eduard; Masdrakis, Vasileios; Mikova, Olya; Nutt, David; Pallanti, Stefano; Pini, Stefano; Ströhle, Andreas; Thibaut, Florence; Vaghi, Matilde M.; Won, Eunsoo; Wedekind, Dirk; Wichniak, Adam; Woolley, Jade; Zwanzger, Peter; Riederer, Peter

doi:10.1080/15622975.2016.1190867

Cited by 268 publications

(190 citation statements)

References 518 publications

(618 reference statements)

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“…80 No changes in BDNF levels were found in a sufficiently large sample of patients with different anxiety disorders, including GAD. 95 However, a small study comparing patients with GAD or MDD with healthy subjects showed doubled plasma levels of BDNF and artemin, a glial-cell-line-derived neurotrophic factor family member, in GAD patients compared with normal controls, whereas depressed patients showed a reduction.…”

Section: Neurochemical Biomarkersmentioning

confidence: 96%

“…However, drawing inferences from the neurochemical composition of plasma on the processes in the brain is not straightforward. 80 Moreover, only a few studies have been conducted on plasma-based pathogenetic and/or treatment predictors in GAD, indicating the further need to explore such potentially valuable approaches. So far, the studies measuring 5-hydroxytryptamine (5-HT, also called serotonin)-related biomarkers have found decreased platelet 5-HT-reuptake-site binding in GAD patients, 81 but unchanged 5-HT binding in lymphocytes as compared with controls.…”

Section: Neurochemical Biomarkersmentioning

confidence: 99%

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Biological Markers of Generalized Anxiety Disorder

Maron¹,

Nutt²

2018

FOC

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Section: Neurochemical Biomarkersmentioning

confidence: 96%

Section: Neurochemical Biomarkersmentioning

confidence: 99%

Biological Markers of Generalized Anxiety Disorder

Maron¹,

Nutt²

2018

FOC

Self Cite

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“…5-HT is a monoamine neurotransmitter produced in serotonergic neurons that project from the dorsal raphe nucleus in the brainstem. It plays a role in the pathogenesis of major depression, bipolar disorder and anxiety (Bandelow et al, 2017;Fakhoury, 2016). PV is a calcium-binding protein that is used to mark a subset of GABAergic interneurons (Le Mageuresse & Monyer, 2013).…”

Section: Introductionmentioning

confidence: 99%

Analysis of Neuropsychiatric Disease‐Related Functional Neuroanatomical Markers in Mice

et al. 2018

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A better alignment of preclinical and clinical neurobiological measures could help improve neuropsychiatric disease therapeutic development. This unit describes a compendium of hypothesis-driven neuroanatomical phenotyping strategies to be employed in genetic mouse models. Using neuropsychiatric disease-based alterations as a guide, these are histological and immunohistochemical methodologies also applied to human tissue. They include quantification assays of neurochemical-, newly born neuron- and glial-cell markers, synaptic proteins, regional volumetrics, dendritic complexity and spine number as well as an index of excitation/inhibition balance. The techniques can be implemented in isolation or to complement concordant behavioral and electrophysiological analyses. Each outcome will provide functional detail necessary to decipher underlying neural circuit abnormalities associated with a brain-related phenotype in mice. Experimental design, timing, anticipated results and potential pitfalls are discussed. © 2018 by John Wiley & Sons, Inc.

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“…Clinically, these receptors are important drug targets for anti‐convulsant, anxiolytic, and sedative–hypnotic agents including benzodiazepines (BZs), barbiturates, alcohol, certain anesthetics and neurosteroids. Underlying deficits in GABAergic neurotransmission occur in a wide variety of neurological disorders such as epilepsy, psychiatric disorders (anxiety [Mohler, ; Nuss, ], depression [Luscher et al, ; Pehrson and Sanchez, ], post‐traumatic stress disorder [Pitman et al, ; Möller et al, ; Trousselard et al, ; Bandelow et al, ]) and neurodevelopmental disorders including autism (Robertson et al, ; Chao et al, ; Coghlan et al, ), Fragile X (Lozano et al, ; Wang et al, ) and schizophrenia (Gonzalez‐Burgos et al, ; Bristow et al, ; Wijtenburg et al, ). Importantly, pathophysiological events including seizures (Scharfman and Brooks‐Kayal, ), ischemic stroke (Carmichael, ; Blicher et al, ; Wu and Sun, ), traumatic brain injury (Guerriero et al, ) and stress can cause adaptive changes in GABA A R neurotransmission, compromising GABAergic inhibition and further hampering recovery.…”

Section: Introductionmentioning

confidence: 99%

GABA type a receptor trafficking and the architecture of synaptic inhibition

Lorenz-Guertin

Jacob

2017

Developmental Neurobiology

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Ubiquitous expression of GABA type A receptors (GABA R) in the central nervous system establishes their central role in coordinating most aspects of neural function and development. Dysregulation of GABAergic neurotransmission manifests in a number of human health disorders and conditions that in certain cases can be alleviated by drugs targeting these receptors. Precise changes in the quantity or activity of GABA Rs localized at the cell surface and at GABAergic postsynaptic sites directly impact the strength of inhibition. The molecular mechanisms constituting receptor trafficking to and from these compartments therefore dictate the efficacy of GABA R function. Here we review the current understanding of how GABA Rs traffic through biogenesis, plasma membrane transport, and degradation. Emphasis is placed on discussing novel GABAergic synaptic proteins, receptor and scaffolding post-translational modifications, activity-dependent changes in GABA R confinement, and neuropeptide and neurosteroid mediated changes. We further highlight modern techniques currently advancing the knowledge of GABA R trafficking and clinically relevant neurodevelopmental diseases connected to GABAergic dysfunction. © 2017 Wiley Periodicals, Inc. Develop Neurobiol 78: 238-270, 2018.

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

Abstract: 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.

Cited by 268 publications

References 518 publications

Biological Markers of Generalized Anxiety Disorder

Biological Markers of Generalized Anxiety Disorder

Analysis of Neuropsychiatric Disease‐Related Functional Neuroanatomical Markers in Mice

GABA type a receptor trafficking and the architecture of synaptic inhibition

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