Evidence map›Paper›PMID 32878083›Full record

ArticleInternational journal of molecular sciences2020

Cerebrospinal Fluid Mitochondrial DNA in Rapid and Slow Progressive Forms of Alzheimer's Disease.

Petar Podlesniy, Franc Llorens, Margalida Puigròs, Nuria Serra, Diego Sepúlveda-Falla, Christian Schmidt, Peter Hermann, Inga Zerr, Ramon Trullas

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

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  9. Targeting mitophagy in neurodegenerative diseases.Nature reviews. Drug discovery · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Petar PodlesniyNeurobiology Unit, Institut d'Investigacions Biomèdiques de Barcelona (CSIC), 08036 Barcelona, Spain.
Franc LlorensCentro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), 08036 Barcelona, Spain.ORCID 0000-0002-9756-7497
Margalida PuigròsNeurobiology Unit, Institut d'Investigacions Biomèdiques de Barcelona (CSIC), 08036 Barcelona, Spain.
Nuria SerraNeurobiology Unit, Institut d'Investigacions Biomèdiques de Barcelona (CSIC), 08036 Barcelona, Spain.
Diego Sepúlveda-FallaInstitute of Neuropathology, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.
Christian SchmidtDepartment of Neurology, Clinical Dementia Center, University Medical School, Georg-August University, 37075 Göttingen, Germany.ORCID 0000-0003-2210-4153
Peter HermannDepartment of Neurology, Clinical Dementia Center, University Medical School, Georg-August University, 37075 Göttingen, Germany.
Inga ZerrDepartment of Neurology, Clinical Dementia Center, University Medical School, Georg-August University, 37075 Göttingen, Germany.ORCID 0000-0002-6722-2463
Ramon TrullasNeurobiology Unit, Institut d'Investigacions Biomèdiques de Barcelona (CSIC), 08036 Barcelona, Spain.ORCID 0000-0001-7951-9881
Biomedical Research Networking Center on Neurodegenerative Diseases · ESGerman Center for Neurodegenerative Diseases · DEBellvitge University Hospital · ESUniversität Hamburg · DE

Funding

Alzheimer Forschung Initiative AFI 12851Bundesministerium für Bildung, Wissenschaft und Forschung IZCentro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas RTInstituto de Salud Carlos III CP16/00041Instituto de Salud Carlos III PI19/00144Instituto de Salud Carlos III PI2016/06Kompetenznetzwerk Degenerative Demenzen, KNDD IZMinisterio de Ciencia e Innovación SAF2017-89791-R
6 · The paper itself

Abstract

Alzheimer's type dementia (AD) exhibits clinical heterogeneity, as well as differences in disease progression, as a subset of patients with a clinical diagnosis of AD progresses more rapidly (rpAD) than the typical AD of slow progression (spAD). Previous findings indicate that low cerebrospinal fluid (CSF) content of cell-free mitochondrial DNA (cf-mtDNA) precedes clinical signs of AD. We have now investigated the relationship between cf-mtDNA and other biomarkers of AD to determine whether a particular biomarker profile underlies the different rates of AD progression. We measured the content of cf-mtDNA, beta-amyloid peptide 1-42 (Aβ), total tau protein (t-tau) and phosphorylated tau (p-tau) in the CSF from a cohort of 95 subjects consisting of 49 controls with a neurologic disorder without dementia, 30 patients with a clinical diagnosis of spAD and 16 patients with rpAD. We found that 37% of controls met at least one AD biomarker criteria, while 53% and 44% of subjects with spAD and rpAD, respectively, did not fulfill the two core AD biomarker criteria: high t-tau and low Aβ in CSF. In the whole cohort, patients with spAD, but not with rpAD, showed a statistically significant 44% decrease of cf-mtDNA in CSF compared to control. When the cohort included only subjects selected by Aβ and t-tau biomarker criteria, the spAD group showed a larger decrease of cf-mtDNA (69%), whereas in the rpAD group cf-mtDNA levels remained unaltered. In the whole cohort, the CSF levels of cf-mtDNA correlated positively with Aβ and negatively with p-tau. Moreover, the ratio between cf-mtDNA and p-tau increased the sensitivity and specificity of spAD diagnosis up to 93% and 94%, respectively, in the biomarker-selected cohort. These results show that the content of cf-mtDNA in CSF correlates with the earliest pathological markers of the disease, Aβ and p-tau, but not with the marker of neuronal damage t-tau. Moreover, these findings confirm that low CSF content of cf-mtDNA is a biomarker for the early detection of AD and support the hypothesis that low cf-mtDNA, together with low Aβ and high p-tau, constitute a distinctive CSF biomarker profile that differentiates spAD from other neurological disorders.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseBiomarkersCase-Control StudiesCohort StudiesDisease ProgressionDNA, MitochondrialFemaleHumansMaleMiddle AgedBiomarkersDNA, MitochondrialAlzheimer’s diseasebiomarkercerebrospinal fluiddigital PCRmitochondrial DNA

Identifiers

PMID32878083
PMCPMC7503553
OpenAlexW3082197292

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.