Evidence map›Paper›PMID 24071439›Full record

ReviewBiochimica et biophysica acta2014

The Alzheimer's disease mitochondrial cascade hypothesis: progress and perspectives.

Russell H Swerdlow, Jeffrey M Burns, Shaharyar M Khan

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 417 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
417citing papers in PubMed, 2 pooled it
19.2field-weighted citation impact, top 1% 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

417 citing papers in PubMed, 2 syntheses or guidelines pooled it, 760 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. GLP-1R agonist semaglutide protects human forebrain organoids from cholesterol-induced neurotoxicity.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  8. SIEVEseq: unified differential expression, variability, and skewness analyses using RNA-Seq data.DNA research : an international journal for rapid publication of reports on genes and genomes · 2026
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  16. FASEB bioAdvances · 2026
    Article
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  20. Review

357 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Russell H SwerdlowDepartments of Neurology and Molecular and Integrative Physiology, and the University of Kansas Alzheimer's Disease Center, University of Kansas School of Medicine, Kansas City, KS, USA; Department of Biochemistry and Molecular Biology, University of Kansas School of Medicine, Kansas City, KS, USA. Electronic address: rswerdlow@kumc.edu.
Jeffrey M BurnsDepartments of Neurology and Molecular and Integrative Physiology, and the University of Kansas Alzheimer's Disease Center, University of Kansas School of Medicine, Kansas City, KS, USA.
Shaharyar M KhanGencia Corporation, Charlottesville, VA, USA.
University of Kansas · USGencia (United States) · US

Funding

University of Kansas Alzheimer's Disease Core CentersP30AG035982 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI BROOKS, WILLIAM M. · 2011 to 2020
$16.6M
NIA NIH HHS P30 AG035982NIA NIH HHS P30AG035982
6 · The paper itself

Abstract

Ten years ago we first proposed the Alzheimer's disease (AD) mitochondrial cascade hypothesis. This hypothesis maintains that gene inheritance defines an individual's baseline mitochondrial function; inherited and environmental factors determine rates at which mitochondrial function changes over time; and baseline mitochondrial function and mitochondrial change rates influence AD chronology. Our hypothesis unequivocally states in sporadic, late-onset AD, mitochondrial function affects amyloid precursor protein (APP) expression, APP processing, or beta amyloid (Aβ) accumulation and argues if an amyloid cascade truly exists, mitochondrial function triggers it. We now review the state of the mitochondrial cascade hypothesis, and discuss it in the context of recent AD biomarker studies, diagnostic criteria, and clinical trials. Our hypothesis predicts that biomarker changes reflect brain aging, new AD definitions clinically stage brain aging, and removing brain Aβ at any point will marginally impact cognitive trajectories. Our hypothesis, therefore, offers unique perspective into what sporadic, late-onset AD is and how to best treat it.

Indexed as

Models, BiologicalSignal TransductionAlzheimer DiseaseAnimalsBiomarkersHumansMitochondriaBiomarkersAgingAlzheimer's diseaseAmyloidBrainDementiaMitochondria

Identifiers

PMID24071439
PMCPMC3962811
OpenAlexW1993160420

What OpenQuestion holds

Textmetadata
LicenceTDM
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.