ArticleAlzheimer's research & therapy2025
Single-cell analysis reveals shared and distinct molecular signatures in brain organoid models of neurodegeneration and neuroinflammation.
Article in Alzheimer's research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Abstract
backgroundAlzheimer’s disease (AD) and Parkinson’s disease (PD) are complex neurodegenerative disorders with common pathological features, but the molecular mechanisms underlying their early stages remain poorly understood. This study aims to elucidate common and divergent changes in cellular processes in the early stages of neurodegeneration and neuroinflammation using brain organoid models.
methodsWe performed a multi-level comparative analysis of single-cell RNA sequencing data from brain organoid models previously designed to mimic specific features of PD- and AD-like pathology, by integrating gene expression, pathway enrichment, molecular network, and cell-cell communication analyses. Given the critical role of neuroinflammation in neurodegenerative disorders, we particularly focused on inflammatory signaling pathways and alterations in cell-cell communication that might drive disease progression.
resultsOur results reveal both common and contrasting changes between the different organoid models, including a common dysregulation of apoptotic pathways in astrocytes, a common upregulation of energy metabolism pathways in neurons, and opposing trends in ribosome-related pathways. Notably, our multi-level analysis identified key inflammatory alterations, including contrasting changes mediated by HMGB1 and shared dysregulation in the MDK signaling pathway. Finally, comparison with post-mortem brain tissue and GWAS data revealed a small set of overlapping significant genes, showing robust shared patterns across different stages of pathology and tissue sources.
conclusionsThese findings provide new insights into the molecular basis of neurodegeneration and neuroinflammation, highlighting diverging and shared alterations between different organoid models and post-mortem brain tissues that may inform follow-up validation and preclinical intervention studies for neurodegenerative disorders.
Indexed as
Identifiers
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.