ReviewJournal of molecular neuroscience : MN2025
Glial Cells in Alzheimer's Disease: Pathogenic Mechanisms and Therapeutic Frontiers.
Review in Journal of molecular neuroscience : MN, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Single-cell RNA sequencing analysis of bone cancer pain model induced by Lewis lung cancer cells in male mice.Annals of medicine · 2026Article
- Neuro-Immune Crosstalk: Molecular Mechanisms, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2026Review
- In vivo imaging of glutamate uncovers the neuroprotective effects of nicotinamide riboside on excitotoxicity in an Alzheimer's mouse model.Alzheimer's research & therapy · 2026Article
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
The rising incidence of brain diseases parallels the global trend of an aging population, with Alzheimer's disease (AD) being a leading neurodegenerative disorder characterized by memory loss, dementia, and cognitive decline. Despite extensive research, current treatments for AD remain largely symptomatic and have had limited success in halting disease progression, thereby shifting attention toward glial cells as promising therapeutic targets due to their emerging roles in AD pathogenesis. Astrocytes are involved in both beneficial and pathological processes in AD, such as cytokine secretion, Aβ removal, metabolic support, and tau pathology, with deficiency resulting in neuroinflammation and excitotoxicity. Microglia have dual functions in AD by phagocytosing amyloid plaques and limiting tau spread in initial phases but may develop a pro-inflammatory, neurodegenerative phenotype with progression of the disease. Oligodendrocytes and their precursors are involved in Aβ generation and myelin homeostasis, and their disturbance is responsible for white matter lesions and cognitive impairment, though their exact mechanisms are less clear. This review also examines emerging therapeutic strategies targeting glial cells, including modulating TREM2 pathways and novel drug candidates. These methods highlight the therapeutic value of the glial cells and provide valuable leads for furthering the treatment of AD by elucidating their changing roles in the course of the disease.
Indexed as
Identifiers
40650861What 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.