Evidence map›Paper›PMID 30471088›Full record

ReviewBritish journal of pharmacology2019

Amyloid precursor protein-mediated mitochondrial regulation and Alzheimer's disease.

M Isabel G Lopez Sanchez, Peter van Wijngaarden, Ian A Trounce

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 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Zebrafish study provides evidence forFrontiers in cellular and infection microbiology · 2026
    Article
  3. Review
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  14. The role of amyloid β in the pathological mechanism of GNE myopathy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022
    Review
  15. Review
  16. Evolving evidence for relationships between periodontitis and systemic diseases: Position paper from the Canadian Dental Hygienists Association.Canadian journal of dental hygiene : CJDH = Journal canadien de l'hygiene dentaire : JCHD · 2022
    Review
  17. Article
  18. Article
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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

3 authors at 1 institution in 1 country.

M Isabel G Lopez SanchezOphthalmology, Department of Surgery, University of Melbourne, Melbourne, VIC, Australia.ORCID 0000-0002-1528-5964
Peter van WijngaardenOphthalmology, Department of Surgery, University of Melbourne, Melbourne, VIC, Australia.ORCID 0000-0002-8800-7834
Ian A TrounceOphthalmology, Department of Surgery, University of Melbourne, Melbourne, VIC, Australia.ORCID 0000-0002-1070-8892
The University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite clear evidence of a neuroprotective physiological role of amyloid precursor protein (APP) and its non-amyloidogenic processing products, APP has been investigated mainly in animal and cellular models of amyloid pathology in the context of Alzheimer's disease. The rare familial mutations in APP and presenilin-1/2, which sometimes drive increased amyloid β (Aβ) production, may have unduly influenced Alzheimer's disease research. APP and its cleavage products play important roles in cellular and mitochondrial metabolism, but many studies focus solely on Aβ. Mitochondrial bioenergetic metabolism is essential for neuronal function, maintenance and survival, and multiple reports indicate mitochondrial abnormalities in patients with Alzheimer's disease. In this review, we focus on mitochondrial abnormalities reported in sporadic Alzheimer's disease patients and the role of full-length APP and its non-amyloidogenic fragments, particularly soluble APPα, on mitochondrial bioenergetic metabolism. We do not review the plethora of animal and in vitro studies using mutant APP/presenilin constructs or experiments using exogenous Aβ. In doing so, we aim to invigorate research and discussion around non-amyloidogenic APP processing products and the mechanisms linking mitochondria and complex neurodegenerative disorders such as sporadic Alzheimer's disease. 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

Alzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsEnergy MetabolismHumansMitochondriaAmyloid beta-Protein Precursor

Identifiers

PMID30471088
PMCPMC6715589
OpenAlexW2901590244

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.