ReviewCurrent neuropharmacology2023
The Role of Neuroglial Metabotropic Glutamate Receptors in Alzheimer's Disease.
Review in Current neuropharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- A systematic review of the neuropathology and memory decline induced by monosodium glutamate in the Alzheimer's disease-like animal model.Frontiers in pharmacology · 2023Pooled it
- Altered Excitation-Inhibition Balance and mGluRInternational journal of molecular sciences · 2026Article
- Recent trends in anti-Alzheimer's potential of novel biologically active isatin analogues: synthetic strategies, structural activity relationship studies and molecular docking insights.Molecular diversity · 2026Review
- The GPCR Connection: Linking Alzheimer's Disease and Glioblastoma.Journal of cellular and molecular medicine · 2026Review
- Neuroglial Function and Hormonal Modulation in Neurodegenerative Diseases: The Influence of Sex Hormones.Cellular and molecular neurobiology · 2026Review
- Curcumin Ameliorates Depressive-like Behaviors by Modulating mGluR2/PGC-1α-Mediated Glutamatergic Homeostasis and Mitochondrial Function.Molecular neurobiology · 2025Article
- Cerebrospinal fluid NPTX2 and [Alzheimer's research & therapy · 2025Article
- G Protein-Coupled Receptor Signaling: Implications and Therapeutic Development Advances in Cancers.MedComm · 2025Review
- Novel Isoindolin-1-one Derivatives as Metabotropic Glutamate Receptor Positive Allosteric Modulators.ACS medicinal chemistry letters · 2025Article
- Unveiling the Interplay: Neurovascular Coupling, Astrocytes and G Protein-Coupled Receptors in Alzheimer's Disease.ACS pharmacology & translational science · 2025Review
- Comprehensive medicinal chemistry survey highlights a portfolio of lead molecules for Alzheimer's disease therapy.Frontiers in chemistry · 2025Review
- Glutamate: Molecular Mechanisms and Signaling Pathway in Alzheimer's Disease, a Potential Therapeutic Target.Molecules (Basel, Switzerland) · 2024Review
- Decoding Neurodegeneration: A Review of Molecular Mechanisms and Therapeutic Advances in Alzheimer's, Parkinson's, and ALS.International journal of molecular sciences · 2024Review
- Effect of Probiotic Therapy on Neuropsychiatric Manifestations in Children with Multiple Neurotransmitter Disorders: A Study.Biomedicines · 2023Article
- Understanding Brain Diseases: From Receptor Dysregulation to Neurodegeneration, Neuroinflammation and Memory Impairment.Current neuropharmacology · 2023Article
- Metabotropic Glutamate Receptor 5 Antagonism Reduces Pathology and Differentially Improves Symptoms in Male and Female Heterozygous zQ175 Huntington's Mice.Frontiers in molecular neuroscience · 2022Article
- Phosphorylation and regulation of group II metabotropic glutamate receptors (mGlu2/3) in neurons.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Glutamate, the major excitatory neurotransmitter in the brain exerts its effects via both ionotropic glutamate receptors and metabotropic glutamate receptors (mGluRs). There are three subgroups of mGluRs, pre-synaptic Group II and Group III mGluRs and post-synaptic Group I mGluRs. mGluRs are ubiquitously expressed in the brain and their activation is poised upstream of a myriad of signaling pathways, resulting in their implication in the pathogenesis of various neurodegenerative diseases including, Alzheimer's Disease (AD). While the exact mechanism of AD etiology remains elusive, β-amyloid (Aβ) plaques and hyperphosphorylated tau tangles remain the histopathological hallmarks of AD. Though less electrically excitable, neuroglia are a major non-neuronal cell type in the brain and are composed of astrocytes, microglia, and oligodendrocytes. Astrocytes, microglia, and oligodendrocytes provide structural and metabolic support, active immune defence, and axonal support and sheathing, respectively. Interestingly, Aβ and hyperphosphorylated tau are known to disrupt the neuroglial homeostasis in the brain, pushing them towards a more neurotoxic state. In this review, we discuss what is currently known regarding the expression patterns of various mGluRs in neuroglia and how Aβ and tau alter the normal mGluR function in the neuroglia and contribute to the pathophysiology of AD.
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.