ccf-mtDNA as a Potential Link Between the Brain and Immune System in Neuro-Immunological Disorders
Open accessAbstract
Fragments of mitochondrial DNA (mtDNA) are released outside the cell and they appear to persist in extracellular fluids as circulating, cell-free, mtDNA (ccf-mtDNA). When compared to nuclear DNA, such a double stranded mtDNA is more resistant to nuclease degradation. In fact, it is stable extracellularly where it can be detected in both plasma and cerebrospinal fluid (CSF), here acting as a potential biomarker in various disorders. In neurological diseases (Alzheimer's disease, Parkinson's disease and end-stage progressive Multiple Sclerosis), a decreased amount of CSF ccf-mtDNA is related with progressive cell dysfunction. This suggests an alteration in neuronal mtDNA levels (mtDNA replication, degradation and depletion) in vulnerable brain regions at early stages of neurodegeneration leading to reduced mtDNA release, which takes place before actual cell death occurs. On the other hand, elevated CSF ccf-mtDNA levels are reported in acute phases of relapsing-remitting Multiple Sclerosis (RRMS). This occurs during acute inflammation, which anticipates the neurodegenerative process. Thus, an increase in inflammatory cells in the affected regions is expected to add on mtDNA release into the CSF. In addition, similarly to bacterial DNA, the non-methylated CpG sites of mtDNA, which activate innate immunity and inflammation, are likely to participate in the molecular mechanisms of disease. Thus, ccf-mtDNA may represent a powerful biomarker for disease screening and prognosis at early stage, although its biological role may extend to generating the neurobiology of disease. The present manuscript discusses recent experimental findings in relationship with clinical evidence comparing neuro-immunological features of neurodegenerative disorders with frankly neuro-infectious diseases.
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Assessing presence of extracellular mitochondria or their fragments by measuring ccf-mtDNA levels could allow on-flight direct estimation of cellular stress to take preventive measures of cumulative damage.
“Assessing the presence of extracellular mitochondria or their fragments by measuring ccf-mtDNA levels could allow on-flight direct estimation of cellular stress to take preventive measures of cumulative damage196,199–206.”
From Key points for the development of antioxidant cocktails to prevent cellular stress and damage caused by reactive oxygen species (ROS) during manned space missions (2021) · cites this paper as [203]
The Introduction (page not provided) describes ccf-mtDNA as a potential biomarker of cell death and tissue injury, and the Neuro-Infections section says its levels may reflect tissue damage or disease severity. The paper does not establish that measuring it provides a direct estimate of cellular stress during flight or enables preventive measures against cumulative damage. (LLM, conf=0.86)
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Nanoparticulate cell-free DNA scavenger for treating inflammatory bone loss in periodontitis
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GDF15 and Cardiac Cells: Current Concepts and New Insights
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Mechanisms of mitochondrial DNA escape and its relationship with different metabolic diseases
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Neurodegeneration and Neuroinflammation in Parkinson’s Disease: a Self-Sustained Loop
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The fate of damaged mitochondrial DNA in the cell
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The role of mitochondria in rheumatic diseases
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Aging: All roads lead to mitochondria
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Expanding and validating the biomarkers for mitochondrial diseases
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Mitochondrial control of innate immune responses
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Mitochondrial DNA: Inherent Complexities Relevant to Genetic Analyses
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Decoding the Rosetta stone of mitonuclear communication
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Mitochondrial DNA and Exercise: Implications for Health and Injuries in Sports
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Pro‐inflammatory role of cell‐free mitochondrial DNA in cardiovascular diseases
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Increased levels of circulating cell-free mtDNA in plasma of late life depression subjects
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Fighting Parkinson’s disease: The return of the mitochondria
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Mitochondrial DAMPs: Key mediators in neuroinflammation and neurodegenerative disease pathogenesis
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Self-citationmtDNA Maintenance and Alterations in the Pathogenesis of Neurodegenerative Diseases
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Hallmarks and Molecular Tools for the Study of Mitophagy in Parkinson’s Disease
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Brain alarm by self-extracellular nucleic acids: from neuroinflammation to neurodegeneration
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Mitochondrial DNA and Neurodegeneration: Any Role for Dietary Antioxidants?
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Developmental Timing of Trauma in Women Predicts Unique Extracellular Vesicle Proteome Signatures
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Bioactive compounds for neuropathic pain: An update on preclinical studies and future perspectives
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Characterization of Mitochondrial DNA Methylation of Alzheimer’s Disease in Plasma Cell-Free DNA
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Intracellular DAMPs in Neurodegeneration and Their Role in Clinical Therapeutics
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Relationship between circulating mitochondrial DNA and microRNA in patients with major depression
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Host mitochondria: more than an organelle in SARS-CoV-2 infection
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Latest assessment methods for mitochondrial homeostasis in cognitive diseases
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Targeted Mitochondrial Epigenetics: A New Direction in Alzheimer’s Disease Treatment
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The war against Alzheimer, the mitochondrion strikes back!
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DNA‐Based Materials Inspired by Natural Extracellular DNA
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Comparison of plasma mitochondrial DNA copy number in asymptomatic and symptomatic COVID-19 patients
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Quantification of Circulating Cell-Free DNA in Idiopathic Parkinson’s Disease Patients
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Is Mitochondria DNA Variation a Biomarker for AD?
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The Potential of cfDNA as Biomarker: Opportunities and Challenges for Neurodegenerative Diseases
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Molecular Pathogenesis and Peripheral Monitoring of Adult Fragile X-Associated Syndromes
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A new hope: Mitochondria, a critical factor in the war against prions
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Circulating Serum Cell-Free Mitochondrial DNA in Amyotrophic Lateral Sclerosis
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- Authors
- Gambardella, S., Limanaqi, F., Ferese, R., Biagioni, F., Campopiano, R., Centonze, D., & Fornai, F.
- Affiliations
- Istituto Neurologico Mediterraneo (IT)
- University of Pisa (IT)
- University of Rome Tor Vergata (IT)
- Corresponding author
- Gambardella, Stefano
- ORCID
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2019-05-09
- Volume
- 10
- Pages
- 1064-1064
- ISSN
- 1664-3224 (ISSN-L)
- PMC
- PMC6520662
- OpenAlex
- W2944647162
- Cited by
- 141
- References
- 87
- Citations by year
- 2026: 12 · 2025: 22 · 2024: 22 · 2023: 27 · 2022: 22 · 2021: 21 · 2020: 13 · 2019: 1 · 2017: 1
- FWCI
- 1.26
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Immunology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
- CINECA IRIS Institutial research information system (University of Pisa) (submittedVersion)
- Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- CINECA IRIS Institutional Research information system (University of Urbino) (submittedVersion)
- Funders
- Ministero della Salute
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Keywords
- circulating cell-free mitochondrial DNA, cerebrospinal fluid biomarkers, neuroinflammation, neurodegeneration, Alzheimer's disease, Parkinson's disease, multiple sclerosis, relapsing-remitting multiple sclerosis, mitochondrial DNA release, CpG sites, innate immunity, central nervous system infection
- MeSH terms
- Cell-Free Nucleic Acids, Animals, Brain, Disease Susceptibility, DNA, Mitochondrial, Gene Expression Regulation, Humans, Immune System, Mitochondria, Nervous System Diseases, Neuroimmunomodulation, Signal Transduction, Biomarkers, Neurodegenerative Diseases, MicroRNAs, Exosomes
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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