Evidence map›Paper›PMID 29036828›Full record

ReviewJournal of Alzheimer's disease : JAD2018

Mitochondria and Mitochondrial Cascades in Alzheimer's Disease.

Russell H Swerdlow

Abstract readReview
In one paragraph

Review in Journal of Alzheimer's disease : JAD, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 507 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
507citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

507 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Effects of the SGLT2 inhibitor dapagliflozin in early Alzheimer's disease: A randomized controlled trial.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Trial
  5. Article
  6. Article
  7. Unveiling the pathogenesis and therapeutic strategies of Alzheimer's disease through cuproptosis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Reframing Alzheimer's Disease Through a Redox-Metabolic Framework.International journal of molecular sciences · 2026
    Review
  12. Review
  13. A peripheral perspective on brain health: vascular and skeletal muscle contributions.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

447 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

1 author.

Russell H SwerdlowUniversity of Kansas Alzheimer's Disease Center and Departments of Neurology, Molecular and Integrative Physiology, and Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, KS, USA.

Funding

University of Kansas Alzheimer's Disease Core CentersP30AG035982 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SWERDLOW, RUSSELL H. · 2011 to 2020
$16.6M
NIA NIH HHS P30 AG035982
6 · The paper itself

Abstract

Decades of research indicate mitochondria from Alzheimer's disease (AD) patients differ from those of non-AD individuals. Initial studies revealed structural differences, and subsequent studies showed functional deficits. Observations of structure and function changes prompted investigators to consider the consequences, significance, and causes of AD-related mitochondrial dysfunction. Currently, extensive research argues mitochondria may mediate, drive, or contribute to a variety of AD pathologies. The perceived significance of these mitochondrial changes continues to grow, and many currently believe AD mitochondrial dysfunction represents a reasonable therapeutic target. Debate continues over the origin of AD mitochondrial changes. Some argue amyloid-β (Aβ) induces AD mitochondrial dysfunction, a view that does not challenge the amyloid cascade hypothesis and that may in fact help explain that hypothesis. Alternatively, data indicate mitochondrial dysfunction exists independent of Aβ, potentially lies upstream of Aβ deposition, and suggest a primary mitochondrial cascade hypothesis that assumes mitochondrial pathology hierarchically supersedes Aβ pathology. Mitochondria, therefore, appear at least to mediate or possibly even initiate pathologic molecular cascades in AD. This review considers studies and data that inform this area of AD research.

Indexed as

Alzheimer DiseaseAnimalsHumansMitochondriaAlzheimer’s diseasebioenergeticscascadecytochrome oxidasemitochondria

Identifiers

PMID29036828
PMCPMC5869994

What OpenQuestion holds

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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 OpenQuestion graph.