Evidence map›Paper›PMID 19757210›Full record

ReviewNeuromolecular medicine2009

Are there common biochemical and molecular mechanisms controlling manganism and parkisonism.

Jerome A Roth

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neuromolecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 83 citations in OpenAlex.

  1. Biomolecules · 2022
    Review
  2. Review
  3. Review
  4. The effects of manganese overexposure on brain health.Neurochemistry international · 2020
    Review
  5. Thiamine Deficiency Modulates p38Neurochemical research · 2020
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Environmental Exposures and Parkinson's Disease.International journal of environmental research and public health · 2016
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

1 author at 1 institution in 1 country.

Jerome A RothDepartment of Pharmacology and Toxicology, University at Buffalo, 11 Cary Hall, Buffalo, NY, 14228, USA. jaroth@buffalo.edu
University at Buffalo, State University of New York · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over the past several decades there has been considerable progress in our basic knowledge as to the mechanisms and factors regulating Mn toxicity. The disorder known as manganism is associated with the preferential accumulation of Mn in the globus pallidus of the basal ganglia which is generally considered to be the major and initial site of injury. Because the area of the CNS comprising the basal ganglia is very complex and dependent on the precise function and balance of several neurotransmitters, it is not surprising that symptoms of manganism often overlap with that of Parkinson's disease. The fact that neurological symptoms and onset of Mn toxicity are quite broad and can vary unpredictably probably reflects specific genetic variance of the physiological and biochemical makeup within the basal ganglia in any individual. Differences in response to Mn overexposure are, thus, likely due to underlying genetic variability which ultimately presents in deviations in both susceptibility as well as the characteristics of the neurological lesions and symptoms expressed. Although chronic exposure to Mn is not the initial causative agent provoking Parkinsonism, there is evidence suggesting that persistent exposure can predispose an individual to acquire dystonic movements associated with Parkinson's disease. As noted in this review, there appears to be common threads between the two disorders, as mutations in the genes, parkin and ATP13A2, associated with early onset of Parkinsonism, may also predispose an individual to develop Mn toxicity. Mutations in both genes appear to effect transport of Mn into the cell. These genetic difference coupled with additional environmental or nutritional factors must also be considered as contributing to the severity and onset of manganism.

Indexed as

Occupational ExposureAnimalsCation Transport ProteinsGenetic Predisposition to DiseaseGenetic VariationGlobus PallidusHumansIronManganeseManganese PoisoningMiceOccupational DiseasesParkinson Disease, SecondaryProton-Translocating ATPasesRatsSolute Carrier Family 11, Member 2ATP13A2 protein, humanCation Transport ProteinsIronManganeseparkin proteinProton-Translocating ATPasesSolute Carrier Family 11, Member 2Ubiquitin-Protein Ligases

Identifiers

PMID19757210
OpenAlexW2073909766

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.