Evidence map›Paper›PMID 36292674›Full record

ReviewGenes2022

Is Mitochondria DNA Variation a Biomarker for AD?

Ruonan Gao, Suk Ling Ma

Open access · goldAbstract readReview
In one paragraph

Review in Genes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Ruonan GaoDepartment of Psychiatry, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China.
Suk Ling MaDepartment of Psychiatry, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China.ORCID 0000-0001-6175-5691
Chinese University of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's Disease (AD) is the most prevalent form of dementia and is characterized by progressive memory loss and cognitive decline. The underlying mechanism of AD has not been fully understood. At present there is no method to detect AD at its early stage. Recent studies indicate that mitochondria dysfunction is related to AD pathogenesis. Altered mitochondria functions are found in AD and influence both amyloid-β (Aβ) and tau pathology. Variations in mitochondria DNA (mtDNA) lead to a change in energy metabolism in the brain and contribute to AD. MtDNA can reflect the status of mitochondria and therefore play an essential role in AD. In this review, we summarize the changes in mtDNA and mtDNA mutations in AD patients and discuss the possibility of mtDNA being a biomarker for the early diagnosis of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBiomarkersDNA, MitochondrialHumansMitochondriaAmyloid beta-PeptidesBiomarkersDNA, MitochondrialAlzheimer’s diseasebiomarkermitochondria DNA

Identifiers

PMID36292674
PMCPMC9601433
OpenAlexW4303685676

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.