Evidence map›Paper›PMID 34248598›Full record

ArticleFrontiers in aging neuroscience2021

Cadmium, an Environmental Contaminant, Exacerbates Alzheimer's Pathology in the Aged Mice's Brain.

Tahir Ali, Amjad Khan, Sayed Ibrar Alam, Sareer Ahmad, Muhammad Ikram, Jun Sung Park, Hyeon Jin Lee, Myeong Ok Kim

Open access · goldAbstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2021. 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
3.0field-weighted citation impact, top 9% 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, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Neurotoxic mechanisms of cadmium in neurodegenerative diseases.Frontiers in cell and developmental biology · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. The Protective Effect of the Supplementation with an Extract fromInternational journal of molecular sciences · 2024
    Article
  14. Article
  15. Zeolite and Neurodegenerative Diseases.Molecules (Basel, Switzerland) · 2024
    Review
  16. Review
  17. Article
  18. Article
  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

8 authors at 1 institution in 2 countries.

Tahir AliDivision of Applied Life Science (BK 21 Four), College of Natural Science, Gyeongsang National University, Jinju, South Korea.
Amjad KhanDivision of Applied Life Science (BK 21 Four), College of Natural Science, Gyeongsang National University, Jinju, South Korea.
Sayed Ibrar AlamDivision of Applied Life Science (BK 21 Four), College of Natural Science, Gyeongsang National University, Jinju, South Korea.
Sareer AhmadDivision of Applied Life Science (BK 21 Four), College of Natural Science, Gyeongsang National University, Jinju, South Korea.
Muhammad IkramDivision of Applied Life Science (BK 21 Four), College of Natural Science, Gyeongsang National University, Jinju, South Korea.
Jun Sung ParkDivision of Applied Life Science (BK 21 Four), College of Natural Science, Gyeongsang National University, Jinju, South Korea.
Hyeon Jin LeeDivision of Applied Life Science (BK 21 Four), College of Natural Science, Gyeongsang National University, Jinju, South Korea.
Myeong Ok KimDivision of Applied Life Science (BK 21 Four), College of Natural Science, Gyeongsang National University, Jinju, South Korea.
Gyeongsang National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cadmium (Cd) is an environmental contaminant, which is a potential risk factor in the progression of aging-associated neurodegenerative diseases. Herein, we have assessed the effects of chronic administration of Cd on cellular oxidative stress and its associated Alzheimer's disease (AD) pathologies in animal models. Two groups of mice were used, one group administered with saline and the other with Cd (1 mg/kg/day; intraperitoneally) for 3 months. After behavioral studies, molecular/biochemical (Immunoblotting, ELISAs, ROS, LPO, and GSH assays) and morphological analyses were performed. We observed an exacerbation of memory and synaptic deficits in chronic Cd-injected mice. Subacute and chronic Cd escalated reactive oxygen species (ROS), suppressed the master antioxidant enzymes, e.g., nuclear factor-erythroid 2-related factor 2 and heme oxygenase-1, and evoked the stress kinase phospho-c-Jun N-terminal kinase 1 signaling pathways, which may escalate AD pathologies possibly associated with amyloidogenic processes. These findings suggest the regulation of oxidative stress/ROS and its associated amyloid beta pathologies for targeting the Cd-exacerbated AD pathogenesis. In addition, these preclinical animal studies represent a paradigm for epidemiological studies of the human population exposed to chronic and subacute administration of Cd, suggesting avoiding environmental contaminants.

Indexed as

Alzheimer’s diseaseantioxidant genes Nrf-2/HO-1Cadmiumneurodegenerationreactive oxygen species

Identifiers

PMID34248598
PMCPMC8263901
OpenAlexW3174554867

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.