Evidence map›Paper›PMID 30675901›Full record

ReviewBritish journal of pharmacology2019

Mitochondrial dysfunction in Alzheimer's disease: Role in pathogenesis and novel therapeutic opportunities.

Judit M Perez Ortiz, Russell H Swerdlow

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 244 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
244citing papers in PubMed, 4 pooled it
17.0field-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

244 citing papers in PubMed, 4 syntheses or guidelines pooled it, 414 citations in OpenAlex.

  1. Pooled it
  2. Systematic review ofFrontiers in aging neuroscience · 2023
    Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Article
  7. Review
  8. Distinct single-nucleus RNA-seq changes among non-neuronal cells in ADNC, LATE-NC, and mixed pathologies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. How Do Amyloid Pathology and Aberrant Neuronal Activity Disrupt Plasticity and Memory in Alzheimer's Disease?The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2026
    Review
  14. Review
  15. Neurotransmitter Systems in Alzheimer's Disease.Current issues in molecular biology · 2026
    Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

184 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

2 authors at 1 institution in 1 country.

Judit M Perez OrtizUniversity of Kansas Alzheimer's Disease Center, Fairway, KS, USA.ORCID 0000-0002-8953-4281
Russell H SwerdlowUniversity of Kansas Alzheimer's Disease Center, Fairway, KS, USA.ORCID 0000-0003-2948-7230
University of Kansas · US

Funding

University of Kansas Alzheimer's Disease Research Center (KU ADRC)P30AG072973 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI Jaime Perales Puchalt · 2021 to 2026
$25.3M
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 P30 AG072973
6 · The paper itself

Abstract

Dysfunction of cell bioenergetics is a common feature of neurodegenerative diseases, the most common of which is Alzheimer's disease (AD). Disrupted energy utilization implicates mitochondria at its nexus. This review summarizes some of the evidence that points to faulty mitochondrial function in AD and highlights past and current therapeutic development efforts. Classical neuropathological hallmarks of disease (β-amyloid and τ) and sporadic AD risk genes (APOE) may trigger mitochondrial disturbance, yet mitochondrial dysfunction may incite pathology. Preclinical and clinical efforts have overwhelmingly centred on the amyloid pathway, but clinical trials have yet to reveal clear-cut benefits. AD therapies aimed at mitochondrial dysfunction are few and concentrate on reversing oxidative stress and cell death pathways. Novel research efforts aimed at boosting mitochondrial and bioenergetic function offer an alternative treatment strategy. Enhancing cell bioenergetics in preclinical models may yield widespread favourable effects that could benefit persons with AD. LINKED ARTICLES: This article is part of a themed section on Therapeutics for Dementia and Alzheimer's Disease: New Directions for Precision Medicine. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.18/issuetoc.

Indexed as

AgingAlzheimer DiseaseAnimalsBrainEnergy MetabolismHumansMitochondria

Identifiers

PMID30675901
PMCPMC6715612
OpenAlexW2913440408

What OpenQuestion holds

Textmetadata
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.