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Non-coding RNAs and Mitochondrial Dysfunction in Alzheimer's Disease: A Systematic Review
Mocrei-Rebrean ȘM, Răzniceanu V, Pintilie SR, Berindan-Neagoe I.. Molecular neurobiology, 2026-09-15
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's disease (AD) is responsible for 70% of dementia cases worldwide, with tau hyperphosphorylation and amyloid-β plaque accumulation representing its core pathological hallmarks. Genetic predisposition, oxidative stress, and neuroinflammation contribute to disease onset and progression. Non-coding ribonucleic acids (ncRNAs) are a class of RNAs which control gene expression and whose dysregulation in AD patients has been linked to amyloid production, neuroinflammation, and mitochondrial dysfunction, which ranges from impaired energy metabolism to disrupted mitochondrial biogenesis and dynamics. Our descriptive systematic review surveyed the involvement of ncRNAs in mitochondrial dysfunction in AD across experimental and clinical literature. We identified multiple microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) that directly regulate mitophagy, mitochondrial biogenesis, mitochondrial autophagic, and apoptotic pathways, mitochondrial dynamics, and protein import mechanisms in AD models. Among the most important candidates demonstrating clinical dysregulation, miR-140 and lncRNA NEAT1 regulate mitophagy, while miR-9, miR-34a, miR-146a, miR-155, and miR-485 are implicated in mitochondrial biogenesis and miR-204 in mitochondrial autophagy. LncRNA BDNF-AS, miR-148a-3p, miR-21-5p, and miR-103a-3p emerged as regulators of the mitochondrial apoptosis pathway with confirmed clinical dysregulation. Multiple ncRNAs control mitochondrial dynamics, of which miR-195, miR-124, and miR-455-3p have also been studied in AD patients. Additionally, several ncRNAs were found to indirectly regulate mitochondrial fission, autophagy, and apoptosis, although the underlying mechanisms require further characterization. Thus, while ncRNA-centered AD research is in its early stages, current mechanistic and translational evidence supports mitochondrially relevant ncRNAs as promising candidates for biomarker and therapeutic development.
Key findings
- Among the most important candidates demonstrating clinical dysregulation, miR-140 and lncRNA NEAT1 regulate mitophagy, while miR-9, miR-34a, miR-146a, miR-155, and miR-485 are implicated in mitochondrial biogenesis and miR-204 in mitochondrial autophagy.
- LncRNA BDNF-AS, miR-148a-3p, miR-21-5p, and miR-103a-3p emerged as regulators of the mitochondrial apoptosis pathway with confirmed clinical dysregulation.
- Multiple ncRNAs control mitochondrial dynamics, of which miR-195, miR-124, and miR-455-3p have also been studied in AD patients.
- Additionally, several ncRNAs were found to indirectly regulate mitochondrial fission, autophagy, and apoptosis, although the underlying mechanisms require further characterization.
- Thus, while ncRNA-centered AD research is in its early stages, current mechanistic and translational evidence supports mitochondrially relevant ncRNAs as promising candidates for biomarker and therapeutic development.
Why it matters
Reviewing lab and clinical studies, the authors identified many non-coding RNAs, molecules that control gene activity, that regulate how mitochondria, the cell's power plants, work in Alzheimer's, including miR-140 and lncRNA NEAT1. Several were also found to be abnormal in patients. The authors say this research is at an early stage, but that these molecules are promising candidates for future biomarkers and treatments.
Study details
- Study designsystematic review
- Evidence strengthHigh
How this study scored 49/100
Published in a peer-reviewed journal, and it is a systematic review of all the studies on the question. Scored zero for sample size, effect reported and studied in people because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Molecular neurobiology) |
| Journal's citation record | 2 / 4 | Molecular Neurobiology: journal h-index 176 (OpenAlex, 2026-10-29) |
| Study design | 12 / 12 | A systematic review of all the studies on the question |
| Strength of evidence | 5 / 5 | Rated “high” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 5 / 5 | 2026 — within 1 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | A review of other studies — randomisation is not credited here |
| Times cited | 0 / 7 | Cited 0 times (OpenAlex, 2026-10-10) |
| Citations per year | 0 / 5 | 0.0 citations a year over 2 year(s) since 2026 |
| Impact for its field and year | 0 / 6 | Cited 0.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 0 / 4 | Cited 0 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Ioana Berindan‐Neagoe: h-index 69 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Iuliu Hațieganu University of Medicine and Pharmacy: institution h-index 257 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 42736501) |
| Free to read | 2 / 2 | Free to read |
| Total | 49 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1007/s12035-026-06198-9
- PubMed: 42736501
- Original source →
- Free full text: Molecular Neurobiology →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
ȘM, M.-R., Răzniceanu, V., Pintilie, SR., & Berindan-Neagoe, I. (2026). Non-coding RNAs and Mitochondrial Dysfunction in Alzheimer's Disease: A Systematic Review. Molecular neurobiology. https://doi.org/10.1007/s12035-026-06198-9
Vancouver
ȘM M.-R, Răzniceanu V, Pintilie SR, Berindan-Neagoe I. Non-coding RNAs and Mitochondrial Dysfunction in Alzheimer's Disease: A Systematic Review. Molecular neurobiology. 2026. doi:10.1007/s12035-026-06198-9. PMID: 42736501.
BibTeX
@article{sm2026-42736501,
author = {ȘM, Mocrei-Rebrean and Răzniceanu, V. and Pintilie, SR. and Berindan-Neagoe, I.},
title = {{Non-coding RNAs and Mitochondrial Dysfunction in Alzheimer's Disease: A Systematic Review}},
journal = {Molecular neurobiology},
year = {2026},
doi = {10.1007/s12035-026-06198-9},
pmid = {42736501},
url = {https://doi.org/10.1007/s12035-026-06198-9}
}
Studies this one cites
Referenced by this study and also in the alzhub library, so you can read them here.