ReviewCurrent neuropharmacology2026
Microglia-Neuron Interactions in Alzheimer's Disease.
Review in Current neuropharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Astragaloside IV Improves Cognitive Impairment in Alzheimer's Mice by Alleviating Neuron PANoptosis.International journal of molecular sciences · 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
8 authors.
Funding
Abstract
Alzheimer's disease (AD) is a progressive disease characterized by significant cognitive decline, posing a substantial threat to life. Neuronal loss and dysfunction are responsible for the cognitive decline and behavioral disturbances observed in AD. Microglia are increasingly recognized for shaping the fate of neurons. However, the role of microglia-neuron interaction in neuronal degeneration of AD remains largely unclear. This review discusses microglia-mediated excessive synaptic pruning and microglia-neuron metabolic coupling in the neuronal degeneration of AD. It also summarizes the role of microglia-neuron interactions in classical pathogenic hypotheses such as the amyloid cascade, tau protein, neuroinflammation, and metal ions. It is found that microglia can serve as protectors of neurons, yet they also exacerbate neuronal damage under stress stimulation. This bidirectional modulation of microglia-neuron interaction provides a novel direction for rescuing AD neurons.
Indexed as
Identifiers
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.