ReviewFrontiers in pharmacology2013
Reduced brain somatostatin in mood disorders: a common pathophysiological substrate and drug target?
Review in Frontiers in pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
75 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Cerebrospinal Fluid Biomarkers in Patients With Unipolar Depression Compared With Healthy Control Individuals: A Systematic Review and Meta-analysis.JAMA psychiatry · 2022Pooled it
- Review
- Neuropeptide therapeutics to repress lateral septum neurons that disable sociability in an autism mouse model.Cell reports. Medicine · 2024Article
- Somatostatin: Linking Cognition and Alzheimer Disease to Therapeutic Targeting.Pharmacological reviews · 2024Review
- Article
- Single-cell genomics and regulatory networks for 388 human brains.Science (New York, N.Y.) · 2024Article
- Article
- Human iN neuronal model of schizophrenia displays dysregulation of chromogranin B and related neuropeptide transmitter signatures.Molecular psychiatry · 2024Article
- Single-cell genomics and regulatory networks for 388 human brains.bioRxiv : the preprint server for biology · 2024Article
- In-silico testing of new pharmacology for restoring inhibition and human cortical function in depression.Communications biology · 2024Article
- Cortisol as a Target for Treating Mental Disorders: A Promising Avenue for Therapy.Mini reviews in medicinal chemistry · 2024Review
- Methylation ofFrontiers in genetics · 2024Article
- Diagnostic Specificity and Association With Cognition of Molecular Alterations in Prefrontal Somatostatin Neurons in Schizophrenia.JAMA psychiatry · 2023Article
- Functional brain region-specific neural spheroids for modeling neurological diseases and therapeutics screening.Communications biology · 2023Article
- Magnetic seizure therapy and electroconvulsive therapy increase aperiodic activity.Translational psychiatry · 2023Article
- Magnetic seizure therapy and electroconvulsive therapy increase aperiodic activity.medRxiv : the preprint server for health sciences · 2023Article
- Single-Cell Transcriptomics Reveals Conserved Regulatory Networks in Human and Mouse Interneuron Development.International journal of molecular sciences · 2023Article
- In-silico EEG biomarkers of reduced inhibition in human cortical microcircuits in depression.PLoS computational biology · 2023Article
- Postnatal Changes of Somatostatin Expression in Hippocampi of C57BL/6 Mice; Modulation of Neuroblast Differentiation in the Hippocampus.Veterinary sciences · 2023Article
- Positive Allosteric Modulation of α5-GABAA Receptors Reverses Stress-Induced Alterations in Dopamine System Function and Prepulse Inhibition of Startle.The international journal of neuropsychopharmacology · 2022Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Our knowledge of the pathophysiology of affect dysregulation has progressively increased, but the pharmacological treatments remain inadequate. Here, we summarize the current literature on deficits in somatostatin, an inhibitory modulatory neuropeptide, in major depression and other neurological disorders that also include mood disturbances. We focus on direct evidence in the human postmortem brain, and review rodent genetic and pharmacological studies probing the role of the somatostatin system in relation to mood. We also briefly go over pharmacological developments targeting the somatostatin system in peripheral organs and discuss the challenges of targeting the brain somatostatin system. Finally, the fact that somatostatin deficits are frequently observed across neurological disorders suggests a selective cellular vulnerability of somatostatin-expressing neurons. Potential cell intrinsic factors mediating those changes are discussed, including nitric oxide induced oxidative stress, mitochondrial dysfunction, high inflammatory response, high demand for neurotrophic environment, and overall aging processes. Together, based on the co-localization of somatostatin with gamma-aminobutyric acid (GABA), its presence in dendritic-targeting GABA neuron subtypes, and its temporal-specific function, we discuss the possibility that deficits in somatostatin play a central role in cortical local inhibitory circuit deficits leading to abnormal corticolimbic network activity and clinical mood symptoms across neurological disorders.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.