Evidence map›Paper›PMID 27340854›Full record

ReviewJournal of Alzheimer's disease : JAD2016

A Bacterial Component to Alzheimer's-Type Dementia Seen via a Systems Biology Approach that Links Iron Dysregulation and Inflammagen Shedding to Disease.

Etheresia Pretorius, Janette Bester, Douglas B Kell

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of Alzheimer's disease : JAD, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Impact on Human Health ofInternational journal of molecular sciences · 2024
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Journal of Alzheimer's disease reports · 2021
    Article
  12. Article
  13. Review
  14. Article
  15. Overdosing on iron: Elevated iron and degenerative brain disorders.Experimental biology and medicine (Maywood, N.J.) · 2020
    Review
  16. Article
  17. Review
  18. Gingipain R1 and Lipopolysaccharide FromFrontiers in immunology · 2020
    Article
  19. Antibiotics, gut microbiota, and Alzheimer's disease.Journal of neuroinflammation · 2019
    Review
  20. Article
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 2 countries.

Etheresia PretoriusDepartment of Physiology, Faculty of Health Sciences, University of Pretoria, Arcadia, South Africa.
Janette BesterDepartment of Physiology, Faculty of Health Sciences, University of Pretoria, Arcadia, South Africa.
Douglas B KellSchool of Chemistry, The University of Manchester, Manchester, Lancs, UK.
University of Pretoria · ZAUniversity of Manchester · GB

Funding

Biotechnology and Biological Sciences Research Council BB/L025752/1Biotechnology and Biological Sciences Research Council BB/M017702/1
6 · The paper itself

Abstract

The progression of Alzheimer's disease (AD) is accompanied by a great many observable changes, both molecular and physiological. These include oxidative stress, neuroinflammation, and (more proximal to cognitive decline) the death of neuronal and other cells. A systems biology approach seeks to organize these observed variables into pathways that discriminate those that are highly involved (i.e., causative) from those that are more usefully recognized as bystander effects. We review the evidence that iron dysregulation is one of the central causative pathway elements here, as this can cause each of the above effects. In addition, we review the evidence that dormant, non-growing bacteria are a crucial feature of AD, that their growth in vivo is normally limited by a lack of free iron, and that it is this iron dysregulation that is an important factor in their resuscitation. Indeed, bacterial cells can be observed by ultrastructural microscopy in the blood of AD patients. A consequence of this is that the growing cells can shed highly inflammatory components such as lipopolysaccharides (LPS). These too are known to be able to induce (apoptotic and pyroptotic) neuronal cell death. There is also evidence that these systems interact with elements of vitamin D metabolism. This integrative systems approach has strong predictive power, indicating (as has indeed been shown) that both natural and pharmaceutical iron chelators might have useful protective roles in arresting cognitive decline, and that a further assessment of the role of microbes in AD development is more than highly warranted.

Indexed as

Bacterial Physiological PhenomenaAlzheimer DiseaseAnimalsHumansIronSystems BiologyIronAlzheimer’s diseasebacteriadormancydysbiosiseryptosisironLPSsystems biologyultramicroscopy

Identifiers

PMID27340854
PMCPMC5325058
OpenAlexW2462662422

What OpenQuestion 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 OpenQuestion graph.