ReviewAging and disease2015
The role of the tripartite glutamatergic synapse in the pathophysiology of Alzheimer's disease.
Review in Aging and disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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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.
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Who cites it
81 citing papers in PubMed.
- A Cross-Region Meta-Analysis and Machine Learning Identifies a 37-Gene Signature Associated with Alzheimer's Disease.Biomedicines · 2026Article
- Repeatability and reproducibility of APT and GluCEST imaging at 5 T: phantom validation and clinical evaluation in patients with brain tumors.BMC medical imaging · 2026Article
- Genetic Inactivation of the Serotonin Transporter Dysregulates Expression of Neurotransmission Genes and Genome-Wide DNA Methylation Levels in the Medial Prefrontal Cortex of Male Rats During Postnatal Development.Developmental neurobiology · 2025Article
- Reactive Astrocytes with Reduced Function of Glutamate Transporters in theACS chemical neuroscience · 2025Article
- Role of mGluR7 in Alzheimer's disease: pathophysiological insights and therapeutic approaches.Inflammopharmacology · 2025Review
- Loss of age-associated increase in mbioRxiv : the preprint server for biology · 2025Article
- Article
- Glutamate: Molecular Mechanisms and Signaling Pathway in Alzheimer's Disease, a Potential Therapeutic Target.Molecules (Basel, Switzerland) · 2024Review
- Sexual dimorphism, altered hippocampal glutamatergic neurotransmission, and cognitive impairment in APP knock-in mice.Journal of Alzheimer's disease : JAD · 2024Article
- Sexual Dimorphism, Altered Hippocampal Glutamatergic Neurotransmission and Cognitive Impairment in APP Knock-In Mice.bioRxiv : the preprint server for biology · 2024Article
- Brain-targeted drug delivery - nanovesicles directed to specific brain cells by brain-targeting ligands.Journal of nanobiotechnology · 2024Review
- Long-lived proteins and DNA as candidate predictive biomarkers for tissue associated diseases.iScience · 2024Article
- Mutual interaction of neurons and astrocytes derived from iPSCs with APP V717L mutation developed the astrocytic phenotypes of Alzheimer's disease.Inflammation and regeneration · 2024Article
- The interaction between ageing and Alzheimer's disease: insights from the hallmarks of ageing.Translational neurodegeneration · 2024Review
- Increased astrocytic GLT-1 expression in tripartite synapses is associated with SCI-induced hyperreflexia.Journal of neurophysiology · 2023Article
- Astrocyte-specific CaBiochemistry and cell biology = Biochimie et biologie cellulaire · 2023Review
- Research Progress on the Etiology and Pathogenesis of Alzheimer's Disease from the Perspective of Chronic Stress.Aging and disease · 2023Review
- Extrasynaptic NMDA receptors in acute and chronic excitotoxicity: implications for preventive treatments of ischemic stroke and late-onset Alzheimer's disease.Molecular neurodegeneration · 2023Review
- Asymmetric dysregulation of glutamate dynamics across the synaptic cleft in a mouse model of Alzheimer's disease.Acta neuropathologica communications · 2023Article
- Prelimbic Cortical Stimulation with L-methionine Enhances Cognition through Hippocampal DNA Methylation and Neuroplasticity Mechanisms.Aging and disease · 2023Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Alzheimer's disease (AD) is the most common form of dementia in individuals over 65 years of age and is characterized by accumulation of beta-amyloid (Aβ) and tau. Both Aβ and tau alter synaptic plasticity, leading to synapse loss, neural network dysfunction, and eventually neuron loss. However, the exact mechanism by which these proteins cause neurodegeneration is still not clear. A growing body of evidence suggests perturbations in the glutamatergic tripartite synapse, comprised of a presynaptic terminal, a postsynaptic spine, and an astrocytic process, may underlie the pathogenic mechanisms of AD. Glutamate is the primary excitatory neurotransmitter in the brain and plays an important role in learning and memory, but alterations in glutamatergic signaling can lead to excitotoxicity. This review discusses the ways in which both beta-amyloid (Aβ) and tau act alone and in concert to perturb synaptic functioning of the tripartite synapse, including alterations in glutamate release, astrocytic uptake, and receptor signaling. Particular emphasis is given to the role of N-methyl-D-aspartate (NMDA) as a possible convergence point for Aβ and tau toxicity.
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