ReviewAging and disease2024
The Role of Glial Cells in Synaptic Dysfunction: Insights into Alzheimer's Disease Mechanisms.
Review in Aging and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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
33 citing papers in PubMed.
- Untangling neuropathic pain: pathophysiological insights and future directions for targeted therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Retinal proteome changes mirror brain pathology and reveal synaptic and cytoskeletal dysfunction in Alzheimer's disease.Acta neuropathologica · 2026Article
- Systematic identification of cell-cell interactions associated with the severity of patients with Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2026Article
- Glial Cells in Behavioral and Psychological Symptoms of Alzheimer's Disease.International journal of molecular sciences · 2026Review
- LCN2/SLC22A17 mediates the phagocytosis of GABAergic synapses by oligodendrocyte progenitor cells and contributes to cancer-induced pain and comorbid anxiety-like behaviors in mice.Acta neuropathologica communications · 2026Article
- From the past to the present: evolving theories in the pathophysiology of normal pressure hydrocephalus.Journal of neurology, neurosurgery, and psychiatry · 2026Review
- Glial Cell Dynamics in Neuroinflammation: Mechanisms, Interactions, and Therapeutic Implications.Biomedicines · 2026Review
- An Acebuche Oil-Enriched Diet Prevents Early-Stage Cerebrovascular Alterations in the 5xFAD Mouse Model of Alzheimer's Disease.Nutrients · 2026Article
- Stage-Dependent Function of Astrocytes in Alzheimer's Disease: A Review.Neuroscience insights · 2026Review
- Editorial: Reviews in non-neuronal cells 2024 & 2025.Frontiers in cellular neuroscience · 2026Article
- Article
- Piracetam attenuates oxidative stress and inflammation-induced neuronal cell death in rats with vascular dementia potentially via the activation of the AMPK/SIRT-1/Nrf-2 signaling pathway.Metabolic brain disease · 2025Article
- Association of qEEG TAR and TBR During Eyes-Open and Eyes-Closed with Plasma Oligomeric Amyloid-β Levels in an Aging Population.Journal of clinical medicine · 2025Article
- Regulatory Genomic Circuitry of Brain Age by Integrative Functional Genomic Analyses.Genomics, proteomics & bioinformatics · 2025Article
- Sex-specific associations of gene expression with Alzheimer's disease neuropathology and ante-mortem cognitive performance.Nature communications · 2025Article
- Review
- Cyclooxygenase-1 deletion in 5 × FAD mice protects against microglia-induced neuroinflammation and mitigates cognitive impairment.Translational neurodegeneration · 2025Article
- Glial reactivity correlates with synaptic dysfunction across aging and Alzheimer's disease.Nature communications · 2025Article
- ABCB1 Gene Polymorphisms and Their Contribution to Cognitive Decline in Mild Cognitive Impairment: A Next-Generation Sequencing Study.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025Article
- Prediction of longitudinal synaptic loss in Alzheimer's disease using tau PET and plasma biomarkers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a devastating neurodegenerative disorder that impacts a substantial number of individuals globally. Despite its widespread prevalence, there is currently no cure for AD. It is widely acknowledged that normal synaptic function holds a key role in memory, cognitive abilities, and the interneuronal transfer of information. As AD advances, symptoms including synaptic impairment, decreased synaptic density, and cognitive decline become increasingly noticeable. The importance of glial cells in the formation of synapses, the growth of neurons, brain maturation, and safeguarding the microenvironment of the central nervous system is well recognized. However, during AD progression, overactive glial cells can cause synaptic dysfunction, neuronal death, and abnormal neuroinflammation. Both neuroinflammation and synaptic dysfunction are present in the early stages of AD. Therefore, focusing on the changes in glia-synapse communication could provide insights into the mechanisms behind AD. In this review, we aim to provide a summary of the role of various glial cells, including microglia, astrocytes, oligodendrocytes, and oligodendrocyte precursor cells, in regulating synaptic dysfunction. This may offer a new perspective on investigating the underlying mechanisms of AD.
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What Socratic 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 Socratic graph.