Blood-derived microRNA signatures associated with hippocampal structure and atrophy rate: findings from the Rhineland Study.
Overview
- Population Health Sciences, German Centre for Neurodegenerative Diseases (DZNE),Bonn, Germany
- Department for Epigenetics and Systems Medicine in Neurodegenerative Diseases, German Center for Neurodegenerative Diseases (DZNE),Göttingen, Germany
- Bioinformatics Unit, German Centre for Neurodegenerative Diseases (DZNE),Göttingen, Germany
- Department for Psychiatry and Psychotherapy, University Medical Center Göttingen,Göttingen, Germany
- Cluster of Excellence MBExC, University of Göttingen & University Medical Center Göttingen,Göttingen, Germany
- Department of Neurology, Faculty of Medicine, University of Bonn,Bonn, Germany
- Institute for Medical Biometry, Informatics and Epidemiology (IMBIE), Faculty of Medicine, University of Bonn,Bonn, Germany
Abstract
MicroRNAs (miRNAs) have been linked to brain disorders, but their relations with hippocampal structure and atrophy remain unexplored. As the hippocampus is pivotal for cognition and dementia, understanding these relations and their specificity for the hippocampus would elucidate miRNA involvement in brain health and neurodegeneration. Here, using population-based data, we cross-sectionally and longitudinally examined the associations of blood-derived miRNAs with left and right hippocampal volume, hippocampal asymmetry, and total brain volume. Expression of miRNAs and their putative target genes was measured at study baseline in whole blood using RNA sequencing. Brain imaging measures were examined at baseline and re-examined 4.60–8.02 years later using 3 T MRI. We investigated miRNA associations with imaging measures cross-sectionally using linear regression and longitudinally using linear mixed-effect models. Cross-sectionally, six miRNAs (miR-199a-3p, miR-199b-3p, miR-155-5p, miR-146a-5p, miR-6859-5p, miR-505-5p) were associated exclusively with left hippocampal volume. Longitudinally, another five miRNAs (miR-361-3p, miR-4473, miR-381-3p, miR-543, miR-370-3p) were associated with left hippocampal, right hippocampal, and total brain atrophy rates. Twenty-one miRNAs were exclusively associated with total brain atrophy rate. In whole blood, miRNAs identified in the cross-sectional analysis targeted genes related to brain development, memory, and synapse assembly. MiRNAs from the longitudinal analysis targeted genes related to axonal and dendritic growth. Several identified miRNAs were previously linked to neurodegeneration. Especially miR-146a-5p and miR-370-3p have been consistently linked to dementia and could be investigated as presymptomatic blood-based biomarkers. The brain-specific functions and interactions with target genes of identified miRNAs could be further investigated to develop therapeutic strategies against neurodegeneration.
Reproduced under the paper's license (CC BY), from the paper cited above.
Code
The paper says that its authors' code is available on request: it was not published with the paper, so there is nothing to verify.
Code availability
The R code used to carry out analyses can be made available upon reasonable request by contacting the authors.
Reproduced under the paper's license (CC BY), from the paper cited above.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none (its code is available on request), so it has no map.
Data
No dataset and no data link were found in the paper.
Data availability
The Rhineland Study’s dataset is not publicly available because of data protection regulations. Access to data can be provided to scientists in accordance with the Rhineland Study’s Data Use and Access Policy. Requests for further information or to access the Rhineland Study’s dataset should be directed to.
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, 8 authors, 3 keywords, 13 MeSH terms, 3 funders, 76 references.
Cite
This paper
Melas, K., Talevi, V., Imtiaz, M. A., Krüger, D. M., Pena-Centeno, T., Fischer, A., Aziz, N. A., & Breteler, M. M. B. (2026). Blood-derived microRNA signatures associated with hippocampal structure and atrophy rate: findings from the Rhineland Study. Molecular psychiatry, 31(9), 5215-5227. https://
BibTeX
@article{melas2026blood,
author = {Melas, Konstantinos and Talevi, Valentina and Imtiaz, Mohammed Aslam and Krüger, Dennis M. and Pena-Centeno, Tonatiuh and Fischer, André and Aziz, N. Ahmad and Breteler, Monique M. B.},
title = {{Blood-derived microRNA signatures associated with hippocampal structure and atrophy rate: findings from the Rhineland Study}},
journal = {Molecular psychiatry},
year = {2026},
month = apr,
volume = {31},
number = {9},
pages = {5215--5227},
publisher = {Springer Nature},
issn = {1359-4184},
doi = {10.1038/
url = {https://
pmid = {42032299},
pmcid = {PMC13441870}
}
RIS
TY - JOUR
AU - Melas, Konstantinos
AU - Talevi, Valentina
AU - Imtiaz, Mohammed Aslam
AU - Krüger, Dennis M.
AU - Pena-Centeno, Tonatiuh
AU - Fischer, André
AU - Aziz, N. Ahmad
AU - Breteler, Monique M. B.
TI - Blood-derived microRNA signatures associated with hippocampal structure and atrophy rate: findings from the Rhineland Study
T2 - Molecular psychiatry
J2 - Mol Psychiatry
PY - 2026
DA - 2026/
VL - 31
IS - 9
SP - 5215
EP - 5227
SN - 1359-4184
PB - Springer Nature
DO - 10.1038/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.1038/
"type": "article-journal",
"title": "Blood-derived microRNA signatures associated with hippocampal structure and atrophy rate: findings from the Rhineland Study",
"container-title": "Molecular psychiatry",
"author": [
{
"family": "Melas",
"given": "Konstantinos"
},
{
"family": "Talevi",
"given": "Valentina"
},
{
"family": "Imtiaz",
"given": "Mohammed Aslam"
},
{
"family": "Krüger",
"given": "Dennis M."
},
{
"family": "Pena-Centeno",
"given": "Tonatiuh"
},
{
"family": "Fischer",
"given": "André"
},
{
"family": "Aziz",
"given": "N. Ahmad"
},
{
"family": "Breteler",
"given": "Monique M. B."
}
],
"container-title-short":
"volume": "31",
"issue": "9",
"page": "5215-5227",
"DOI": "10.1038/
"PMID": "42032299",
"PMCID": "PMC13441870",
"ISSN": "1359-4184",
"publisher": "Springer Nature",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
4,
24
]
]
}
}
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:10.1016/j.ebiom.2026.106289 [code]
- DNA methylation signatures of bilateral hippocampal volume, asymmetry and atrophy: a cross-omics analysis in the general population.Journal: EBioMedicineIn common: structural MRI / diffusion, 2 references, 2 authors
- [2] doi:10.1186/s13073-026-01702-1
- Tandem repeat polymorphisms are associated with brain structure: results of two large population-based studies.Journal: Genome medicineIn common: structural MRI / diffusion, 2 references, author Monique M.B. Breteler
- [3] doi:10.1111/acel.70659
- Effects of Physical Activity on Brain White Matter Integrity Are Region-, Dose-, and Age-Dependent: Findings From the Population-Based Rhineland Study.Journal: Aging cellIn common: structural MRI / diffusion, 2 references, author Monique M.B. Breteler
- [4] doi:10.64898/2026.08.12.26360241
- Diffusion kurtosis imaging (gen)omics unravels mechanisms of cerebral small vessel diseaseJournal: medRxiv (preprint)In common: Alzheimer's / dementia, structural MRI / diffusion, cellular / molecular, 1 reference, author Monique M.B. Breteler
- [5] doi:10.1038/s41467-026-76956-9 [code]
- Innervated human cardiac muscle model reveals sympathetic drivers of KCNH2-associated arrhythmias.Journal: Nature communicationsIn common: 1 reference, author Dennis Krüger
- [6] doi:10.1016/j.nbd.2026.107379 [code]
- DYRK1A and Parkinson's disease, facts and hypotheses.Journal: Neurobiology of diseaseIn common: Alzheimer's / dementia, cellular / molecular, 2 references
- [7] doi:10.1186/s40478-026-02228-8
- microRNA-132 attenuates inflammation in induced pluripotent stem cell-derived microglia from Alzheimer's disease patients.Journal: Acta neuropathologica communicationsIn common: Alzheimer's / dementia, cellular / molecular, 2 references
- [8] doi:10.3390/biom16060776
- Alterations of Cerebral Extracellular Vesicle microRNA Profiling Potentially Disrupts Brain Homeostasis Following Myocardial Infarction.Journal: BiomoleculesIn common: cellular / molecular, 3 references
- [9] doi:10.1162/imag.a.1183 [code]
- Learning-based segmentation of diffusion-weighted MR images with arbitrary &
lt;i& gt;q& lt;/ i& gt;-space samplings. Journal: Imaging neuroscience (Cambridge, Mass.)In common: structural MRI / diffusion, 2 references - [10] doi:10.1002/alz.71609
- Cortical gray-white matter contrast alterations precede amyloid-β positivity and macrostructural changes in older adults without dementia.Journal: Alzheimer's & dementia : the journal of the Alzheimer's AssociationIn common: Alzheimer's / dementia, structural MRI / diffusion, 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.
