Microglia Mitochondria Support Neuronal Maturation via Metabolic and Transcriptional Reprogramming in Human 3D In Vitro Brain Model.
Overview
- Department of Biomedical Engineering, University of Cincinnati, Cincinnati, Ohio, USA
- Neuroscience Graduate Program, College of Medicine, University of Cincinnati, Cincinnati, Ohio, USA
Abstract
Autism Spectrum Disorder (ASD) is a neurodevelopmental condition characterized by disrupted neuronal circuit maturation. Emerging evidence implicates microglial function and mitochondrial regulation as contributors to ASD‐associated biology, yet the mechanisms linking these processes to neuronal development remain poorly defined. Neuronal maturation requires tightly coordinated metabolic and transcriptional remodeling, in which mitochondria play a central role in regulating the developmental tempo and metabolic identity, while microglia modulate neuronal synaptic network maturation; however, whether microglia influence neuronal development through direct mitochondrial contributions remains unknown. Here, using a 3D human in vitro brain model, it is shown that microglial mitochondria can act as transferable cues that promote metabolic, mitochondria‐dynamic, and transcriptional aspects of neuronal maturation. Neurons treated with microglial mitochondria exhibited enhanced oxidative metabolism, improved mitochondrial dynamics, and activation of gene programs associated with nervous system development and neurogenesis. These effects are accompanied by increased expression of dendritic maturation markers, supporting the view that transferred mitochondria can contribute to the regulation of neuronal state. However, full structural and synaptic maturation required the combined action of microglia‐derived mitochondria and secreted signaling factors. Together, this study identified microglial mitochondrial transfer as a contributor to neuronal maturation with potential relevance to developmental trajectories disrupted in ASD.
Reproduced under the paper's license (CC BY), from the paper cited above.
Code
The paper links to its data, not to its authors' code: see the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none, so it has no map.
Data
Datasets cited
- geo:GSE319314, at NCBI GEO; found in “Data Availability Statement”
Other data links
- ncbi.nlm.nih.gov/
geo , NCBI; found in “Data Availability Statement”
Data Availability Statement
All data generated or analyzed during this study are included in this article (and its supporting information files). This study's mRNA sequencing data set was deposited in the GEO repository database (https://
Reproduced under the paper's license (CC BY), from the paper cited above.
Versions
The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.
Version 1, 30 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 5 authors, 5 keywords, 9 MeSH terms, 4 funders, 56 references.
Cite
This paper
Sterben, S. P., Anamala, C. C., Kansakar, S. B. S., Koduri, V., & Liaudanskaya, V. (2026). Microglia Mitochondria Support Neuronal Maturation via Metabolic and Transcriptional Reprogramming in Human 3D In Vitro Brain Model. Advanced science (Weinheim, Baden-Wurttemberg, Germany), 13(25), e08815. https://
BibTeX
@article{sterben2026micr
author = {Sterben, Sydney P and Anamala, Charitha C and Kansakar, Sahan B S and Koduri, Vaishnavi and Liaudanskaya, Volha},
title = {{Microglia Mitochondria Support Neuronal Maturation via Metabolic and Transcriptional Reprogramming in Human 3D In Vitro Brain Model}},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
year = {2026},
month = mar,
volume = {13},
number = {25},
pages = {e08815},
publisher = {Wiley},
issn = {2198-3844},
doi = {10.1002/
url = {https://
pmid = {41823577},
pmcid = {PMC13137835}
}
RIS
TY - JOUR
AU - Sterben, Sydney P
AU - Anamala, Charitha C
AU - Kansakar, Sahan B S
AU - Koduri, Vaishnavi
AU - Liaudanskaya, Volha
TI - Microglia Mitochondria Support Neuronal Maturation via Metabolic and Transcriptional Reprogramming in Human 3D In Vitro Brain Model
T2 - Advanced science (Weinheim, Baden-Wurttemberg, Germany)
J2 - Adv Sci (Weinh)
PY - 2026
DA - 2026/
VL - 13
IS - 25
SP - e08815
SN - 2198-3844
PB - Wiley
DO - 10.1002/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.1002/
"type": "article-journal",
"title": "Microglia Mitochondria Support Neuronal Maturation via Metabolic and Transcriptional Reprogramming in Human 3D In Vitro Brain Model",
"container-title": "Advanced science (Weinheim, Baden-Wurttemberg, Germany)",
"author": [
{
"family": "Sterben",
"given": "Sydney P"
},
{
"family": "Anamala",
"given": "Charitha C"
},
{
"family": "Kansakar",
"given": "Sahan B S"
},
{
"family": "Koduri",
"given": "Vaishnavi"
},
{
"family": "Liaudanskaya",
"given": "Volha"
}
],
"container-title-short":
"volume": "13",
"issue": "25",
"page": "e08815",
"DOI": "10.1002/
"PMID": "41823577",
"PMCID": "PMC13137835",
"ISSN": "2198-3844",
"publisher": "Wiley",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
3,
13
]
]
}
}
Similar papers
The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.
- [1] doi:10.3389/ftox.2026.1816944 [code]
- Neurodevelopmental outcomes relevant to autism in juvenile mice exposed to PCB 11 in the maternal diet throughout gestation and lactation.Journal: Frontiers in toxicologyIn common: autism, 3 references
- [2] doi:10.1016/j.cell.2026.07.023
- Metabolic atlas of early human cortex reveals glycolytic remodeling and pentose phosphate pathway control of cell fate transitions.Journal: CellIn common: 3 references
- [3] doi:10.1186/s13293-026-00982-x
- Sex differences in ferroptosis-related vulnerability to autism-like deficits in the adolescent medial prefrontal cortex following embryonic valproic acid exposure.Journal: Biology of sex differencesIn common: autism, 2 references
- [4] doi:10.3390/genes17080874 [code]
- Multi-Omic Analysis of Cerebrospinal Fluid Metabolites in Autism Spectrum Disorder: Biomarker Identification, Metabolic Genetics Insights, and Network Toxicology.Journal: GenesIn common: autism, 2 references
- [5] doi:10.1186/s12974-026-03739-w [code]
- Sex specific effects of adoptive Tregs transfer on the brain and periphery in maternal immune activation offspring rescuing immune dysregulation.Journal: Journal of neuroinflammationIn common: autism, 2 references
- [6] doi:10.3389/fnmol.2026.1844343
- Molecular abnormalities scale across three models of cerebral injury.Journal: Frontiers in molecular neuroscienceIn common: 2 references
- [7] doi:10.1002/adhm.202503457 [code]
- A 3D Human Neuron-on-Chip Platform to Monitor Neuronal Injury Responses.Journal: Advanced healthcare materialsIn common: 2 references
- [8] doi:10.1111/acel.70616
- Transcriptomic Evidence of Mitochondrial Double-Stranded RNA Accumulation in Brain Aging and Alzheimer's Disease.Journal: Aging cellIn common: 2 references
- [9] doi:10.1038/s41467-026-71391-2 [code]
- Accelerating Leigh syndrome drug discovery through deep learning screening in brain organoids.Journal: Nature communicationsIn common: 2 references
- [10] doi:10.1186/s11689-026-09713-0 [code]
- DRP1 mutations associated with EMPF1 encephalopathy perturb the transcriptional profile and maturation of cortical neurons.Journal: Journal of neurodevelopmental disordersIn common: 2 references
Contribute
The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.
Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.
Claim this paper
Correct its record
Say what each link of this record is, remove the ones that are not the paper's, add the ones that are missing. The correction becomes a new version of the record, in its Versions section.
Request its removal
To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).
Discussion, reproductions, activity
Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.
Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.
Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.
