Evidence map›Paper›PMID 36224040›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2023

The role of mitochondrial genome abundance in Alzheimer's disease.

Nadia V Harerimana, Devashi Paliwali, Carmen Romero-Molina, David A Bennett, Judy Pa, Alison Goate, Russell H Swerdlow, Shea J Andrews

Open access · hybridAbstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Mitochondrial haplogroups, but not heteroplasmy, are associated with midlife cognitive function.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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  9. Review
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  15. Inhibiting mtDNA transcript translation alters Alzheimer's disease-associated biology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
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  19. Review
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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

8 authors at 6 institutions in 2 countries.

Nadia V HarerimanaRonald M. Loeb Center for Alzheimer's Disease, Department of Genetics & Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Devashi PaliwaliDepartment of Genome Sciences, John Curtin School of Medical Research, The Australian National University, Canberra, Australian Capital Territory, Australia.
Carmen Romero-MolinaRonald M. Loeb Center for Alzheimer's Disease, Department of Genetics & Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
David A BennettRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, Illinois, USA.
Judy PaDepartment of Neurosciences, Alzheimer's Disease Cooperative Study (ADCS), University of California, San Diego, California, USA.
Alison GoateRonald M. Loeb Center for Alzheimer's Disease, Department of Genetics & Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Russell H SwerdlowUniversity of Kansas Alzheimer's Disease Research Center, Kansas City, Kansas, USA.
Shea J AndrewsRonald M. Loeb Center for Alzheimer's Disease, Department of Genetics & Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Icahn School of Medicine at Mount Sinai · USAustralian National University · AURush University Medical Center · USUniversity of California, San Diego · USUniversity of California, San Francisco · USUniversity of Kansas · US

Funding

SUPPLEMENT TO RUSH ALZHEIMERS DISEASE CENTER COREP30AG010161 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 1991 to 2020
$49.1M
EPIDEMIOLOGY OF NEURAL RESERVE AND NEUROBIOLOGY IN AGINGR01AG017917 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 2001 to 2023
$43.3M
University of Kansas Alzheimer's Disease Research Center (KU ADRC)P30AG072973 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI Mohammad Haeri · 2021 to 2026
$25.3M
Rush Alzheimer's Disease Research CenterP30AG072975 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI Lisa L Barnes, Julie A. Schneider · 2021 to 2026
$24.7M
RISK FACTORS, PATHOLOGY, AND CLINICAL EXPRESSIONS OF ADR01AG015819 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 1998 to 2024
$21.4M
Multi-omic network-directed proteoform discovery, dissection and functional validation to prioritize novel AD therapeutic targetsU01AG061356 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BENNETT, DAVID ALAN, DE JAGER, PHILIP L · 2018 to 2022
$13.7M
Pathway discovery, validation and compound identification for Alzheimer's disease - SupplementU01AG046152 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BENNETT, DAVID ALAN, DE JAGER, PHILIP L · 2013 to 2017
$13.6M
Mechanistic Basis of the mtDNA Haplogroup J-Alzheimer's Disease AssociationR01AG061194 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SWERDLOW, RUSSELL H. · 2019 to 2023
$1.9M
National Institutes of Health - National Institute on Aging P30AG072973National Institutes of Health - National Institute on Aging P30AG10161National Institutes of Health - National Institute on Aging P30AG72975National Institutes of Health - National Institute on Aging R01AG054617National Institutes of Health - National Institute on Aging R01AG061194National Institutes of Health - National Institute on Aging R01AG15819National Institutes of Health - National Institute on Aging R01AG17917National Institutes of Health - National Institute on Aging U01AG46152National Institutes of Health - National Institute on Aging U01AG61356NIA NIH HHS R01 AG061194
6 · The paper itself

Abstract

Mitochondrial dysfunction is an early and prominent feature of Alzheimer's disease (AD), with impaired energy metabolism preceding the onset of clinical symptoms. Here we propose an update to the mitochondrial dysfunction hypothesis of AD based on recent results examining the role of mitochondrial genome abundance in AD. In a large post mortem study, we show that lower brain mitochondrial genome abundance is associated with a greater odds of AD neuropathological change and worse cognitive performance. We hypothesize that lower mitochondrial genome abundance impairs mitochondrial function by reducing mitochondrial bioenergetics, thereby impacting neuronal and glial cell function. However, it remains to be determined if mitochondrial dysfunction causes, mediates, or is a by-product of AD pathogenesis. Additional support for this hypothesis will be generated by linking peripheral blood mitochondrial genome abundance to AD and establishing clinical trials of compounds that upregulate total mitochondrial genome abundance or boost mitochondrial mass.

Indexed as

Alzheimer DiseaseGenome, MitochondrialBrainEnergy MetabolismHumansMitochondriaAlzheimer's diseasehaplogroupmitochondrial DNA copy numbermitochondrial dysfunctionmitochondrial genome abundancemitochondrial heteroplasmy

Identifiers

PMID36224040
PMCPMC13043242
OpenAlexW4304806923

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.