ReviewFrontiers in aging neuroscience2016
Implications of GABAergic Neurotransmission in Alzheimer's Disease.
Review in Frontiers in aging neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers, 6 of them syntheses 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
151 citing papers in PubMed, 6 syntheses or guidelines pooled it, 279 citations in OpenAlex.
- Use of Drugs Affecting GABAMolecular neurobiology · 2025Pooled it
- The Footprint ofCurrent Alzheimer research · 2025Pooled it
- Magnetic resonance spectroscopy with transcranial direct current stimulation to explore the underlying biochemical and physiological mechanism of the human brain: A systematic review.Human brain mapping · 2021Pooled it
- A Systematic Review of Long-Interval Intracortical Inhibition as a Biomarker in Neuropsychiatric Disorders.Frontiers in psychiatry · 2021Pooled it
- The Influence of Nutrition in Alzheimer's Disease: Neuroinflammation and the Microbiome vs. Transmissible Prion.Frontiers in neuroscience · 2021Pooled it
- Evaluation of Metabolic and Synaptic Dysfunction Hypotheses of Alzheimer's Disease (AD): A Meta-Analysis of CSF Markers.Current Alzheimer research · 2018Pooled it
- Trial
- Regional juxtacortical microstructural changes and gene expression provide insights into neurodegeneration in Alzheimer's disease.Translational psychiatry · 2026Article
- Environmental Factors Drive Neurodegenerative Diseases Through Glutamate Excitotoxicity: A Convergent Mechanistic Pathway.Neuroscience bulletin · 2026Review
- Neuroprotective Effects of Berberine Chloride Against the Aluminium Chloride-Induced Alzheimer's Disease in Zebra Fish Larvae.Molecular biotechnology · 2026Article
- Computer-aided Drug Design for Alzheimer's Disease: Recent Advancements and Future Perspectives.Current topics in medicinal chemistry · 2026Review
- Lysophosphatidylcholines are associated with amyloidosis in early stages of Alzheimer's disease.Nature aging · 2026Article
- Neurotransmitters and Immunity: Molecular Mechanisms, Biological Functions, Diseases, and Potential Therapeutic Targets.MedComm · 2025Review
- The medial septum-hippocampus-lateral septum circuitry in spatial memory: linking healthy function to early Alzheimer's disease and translational opportunities.Translational neurodegeneration · 2025Review
- Beyond epilepsy: The expanding role of valproic acid in Alzheimer disease therapy - a review.The Journal of pharmacology and experimental therapeutics · 2025Review
- miR-361-5p contributes to the pathogenesis of Alzheimer's disease.Scientific reports · 2025Article
- Functional discrimination of CSF from Alzheimer's patients in a brain on chip platform.Scientific reports · 2025Article
- Neurophysiological correlates of modifiable dementia risk factors in cognitively unimpaired older adults.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
- Chemoreflex function in pulmonary diseases - A review.The Journal of physiology · 2025Review
- Transcriptomic analyses of human brains with Alzheimer's disease identified dysregulated epilepsy-causing genes.Epilepsy & behavior : E&B · 2025Article
91 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
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is characterized pathologically by the deposition of β-amyloid peptides (Aβ) and the accumulation of neurofibrillary tangles (NFTs) composed of hyper-phosphorylated tau. Regardless of the pathological hallmarks, synaptic dysfunction is widely accepted as a causal event in AD. Of the two major types of synapses in the central nervous system (CNS): glutamatergic and GABAergic, which provide excitatory and inhibitory outputs respectively, abundant data implicate an impaired glutamatergic system during disease progression. However, emerging evidence supports the notion that disrupted default neuronal network underlies impaired memory, and that alterations of GABAergic circuits, either plays a primary role or as a compensatory response to excitotoxicity, may also contribute to AD by disrupting the overall network function. The goal of this review is to provide an overview of the involvement of Aβ, tau and apolipoprotein E4 (apoE4), the major genetic risk factor in late-onset AD (LOAD), in GABAergic neurotransmission and the potential of modulating the GABAergic function as AD therapy.
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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.