ReviewMolecular psychiatry2021
Altered GABA-mediated information processing and cognitive dysfunctions in depression and other brain disorders.
Review in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
129 citing papers in PubMed, 1 synthesis or guideline pooled it, 229 citations in OpenAlex.
- Identification of risk loci for postpartum depression in a genome-wide association study.Psychiatry and clinical neurosciences · 2024Pooled it
- Efficacy of empagliflozin as adjunctive therapy to citalopram in major depressive disorder: a randomized double-blind, placebo-controlled clinical trial.BMC psychiatry · 2024Trial
- Parvalbumin interneurons under stress: converging mechanisms of vulnerability.The international journal of neuropsychopharmacology · 2026Review
- Beyond the sugar coating: mucin-type O-Glycosylation as an underappreciated player in brain function and disease.Molecular psychiatry · 2026Review
- Standardized chronic restraint stress protocols reveal dynamic evolution of behavioral adaptations in male mice: implications for translational neuroscience.Molecular psychiatry · 2026Article
- Depression in neurodegenerative disease: neurobiological mechanisms and emerging treatments.Molecular psychiatry · 2026Review
- Paradigm Shift of Microbiota-gut-brain Axis During Aging: Potential Role of Probiotics to Improve Cognitive Decline.Probiotics and antimicrobial proteins · 2026Review
- The comparative ameliorating effects of an amorphous formula of curcumin and α-glycosyl isoquercitrin on hippocampal dysfunction in a rat gulf war illness model.Metabolic brain disease · 2026Article
- Review
- Influences of subtle NMDA receptor blockade and allosteric modulation of α5 GABAA receptors on reward-related impulsivity in rats.Psychopharmacology · 2026Article
- Trihexyphenidyl Ameliorates Depression-like Behaviors in Adult Zebrafish Exposed to Chronic Unpredictable Stress, Consistent with Regulation of the MAPK Signaling Pathway.Biomolecules · 2026Article
- A Novel Polygenic Risk Score Indexing Somatostatin-Expressing Inhibitory Neurons Predicts Somatostatin-Expressing Cell Proportions and Severity of Symptoms in Late-Life Depression.Biological psychiatry global open science · 2026Article
- Insomnia: the gut microbiome connection, prospects for probiotic and postbiotic therapies, and future directions.Journal of advanced research · 2026Review
- Exploratory study of plasma GFAP and GAD65-Ab levels in children with ADHD.Italian journal of pediatrics · 2026Article
- Digital Twin Brain simulation and manipulation of a functional brain network underlying mental illness.bioRxiv : the preprint server for biology · 2026Article
- Genetic liability to addiction underlies comorbid bipolar and substance use disorders.medRxiv : the preprint server for health sciences · 2026Article
- Oral Supplementation With a Bovine Thymus Extract Reduces Neuronal Excitability in Aging Mice.FASEB bioAdvances · 2026Article
- Age-specific alterations in gut microbiota-plasma metabolome networks in first-episode, drug-naïve major depressive disorder: adolescent versus adult patients.Frontiers in microbiology · 2026Article
- Selective magnetic stimulation downregulates the GABAMolecular psychiatry · 2026Article
- When pain becomes self: limbic-default mode network hyperconnectivity predicts microvascular decompression failure in trigeminal neuralgia.Brain communications · 2026Article
69 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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cognitive dysfunctions, including impaired attention, learning, memory, planning and problem solving, occur in depressive episodes, often persist during remission, predict relapse, worsen with recurrent episodes, and are not treated by current antidepressants or other medications. Cognitive symptoms are also present in other psychiatric disorders, are a hallmark of aging, and define several late-life disorders, including Alzheimer's disease. This pervasive occurrence suggests either a non-specific outcome of a diseased brain, or a shared underlying pathology contributing to this symptom dimension. Recent findings suggest a role for altered GABAergic inhibition in cognitive symptoms. Cellular, molecular and biochemical studies in human subjects report changes affecting the gamma-amino butyric acid (GABA) system, specifically somatostatin-expressing (SST+) GABAergic interneurons, across brain disorders and during aging. SST+ neurons gate excitatory input onto pyramidal neurons within cortical microcircuits. Experimentally reducing the function of these neurons affects excitatory signal-to-noise ratio, reduces synchronized cellular and neural activity, and leads to cognitive dysfunctions. Conversely, augmenting SST+ cell post-synaptic α5-GABA-A receptor activity has pro-cognitive efficacy in stress and aging models. Together, this suggests that reduced signaling of the SST+ neuron/α5-GABA-A receptor pathway contributes to cognitive dysfunctions, and that it represents a novel therapeutic target for remediating mood and cognitive symptoms in depression, other psychiatric disorders and during aging.
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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.