Evidence map›Paper›PMID 27551259›Full record

ReviewFrontiers in molecular neuroscience2016

Ammonia as a Potential Neurotoxic Factor in Alzheimer's Disease.

Aida Adlimoghaddam, Mohammad G Sabbir, Benedict C Albensi

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in molecular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

54 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
  2. Article
  3. The role of ammonia in chronic liver disease.Hepatology communications · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Pathway enrichment in genome-wide analysis of longitudinal Alzheimer's disease biomarker endophenotypes.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  17. Article
  18. Review
  19. Article
  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 1 institution in 1 country.

Aida AdlimoghaddamDivision of Neurodegenerative Disorders, St. Boniface Hospital Research Winnipeg, MB, Canada.
Mohammad G SabbirDivision of Neurodegenerative Disorders, St. Boniface Hospital Research Winnipeg, MB, Canada.
Benedict C AlbensiDivision of Neurodegenerative Disorders, St. Boniface Hospital ResearchWinnipeg, MB, Canada; Department of Pharmacology & Therapeutics, University of ManitobaWinnipeg, MB, Canada.
St. Boniface Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ammonia is known to be a potent neurotoxin that causes severe negative effects on the central nervous system. Excessive ammonia levels have been detected in the brain of patients with neurological disorders such as Alzheimer disease (AD). Therefore, ammonia could be a factor contributing to the progression of AD. In this review, we provide an introduction to the toxicity of ammonia and putative ammonia transport proteins. We also hypothesize how ammonia may be linked to AD. Additionally, we discuss the evidence that support the hypothesis that ammonia is a key factor contributing to AD progression. Lastly, we summarize the old and new experimental evidence that focuses on energy metabolism, mitochondrial function, inflammatory responses, excitatory glutamatergic, and GABAergic neurotransmission, and memory in support of our ammonia-related hypotheses of AD.

Indexed as

Alzheimer diseaseammoniaammonia transportersenergy metabolismGABAergicglutamatergicmitochondrial dysfunctiontoxicity

Identifiers

PMID27551259
PMCPMC4976099
OpenAlexW2495915470

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.