ReviewNeuroscience bulletin2026
A Question of Origins: Non-neuronal Sources of Amyloid-β.
Review in Neuroscience bulletin, 2026. 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.
- Beyond the Wiring: White Matter as a Dynamic Regulator of Brain Function and Disease.Neuroscience bulletin · 2026Review
- Neuroinflammation in Alzheimer's and Parkinson's diseases: pathogenic mechanisms and therapeutic strategies.Translational neurodegeneration · 2026Review
- Investigating Alzheimer's Disease-Associated Genes Using Differential Splicing Frequency Analysis.Cells · 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyloid-β (Aβ) plaques and neurofibrillary tau tangles are hallmarks of Alzheimer's disease (AD). While the intracellular localization of tau tangles within neurons nominates them as the primary producers of tau, the cellular origin of Aβ is less clear as plaques accumulate extracellularly. Neurons have been considered the sole source of Aβ, leading to the generation of many AD animal models expressing familial AD protein variants specifically in neurons. However, emerging evidence showed that non-neuronal cells abundantly express amyloid precursor protein (APP) and its processing machinery. Among these, oligodendrocytes (OLs) exhibit the highest expression of amyloidogenic components, produce Aβ, and contribute to plaque burden in vivo. Here, we highlight reports on non-neuronal Aβ production in the context of AD and the function of APP processing in these cells. Understanding Aβ processing in non-neuronal cells might enable the identification of novel therapeutic targets, especially in humans whose brain structures differ greatly from animal models.
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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.