Evidence map›Paper›PMID 32194507›Full record

ArticleFrontiers in endocrinology2020

Adiponectin Paradox in Alzheimer's Disease; Relevance to Amyloidogenic Evolvability?

Masaaki Waragai, Gilbert Ho, Yoshiki Takamatsu, Ryoko Wada, Shuei Sugama, Takato Takenouchi, Eliezer Masliah, Makoto Hashimoto

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2020. 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
3.3field-weighted citation impact, top 7% 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, 29 citations in OpenAlex.

  1. Article
  2. Review
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  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Genes · 2022
    Article
  12. Article
  13. An Explanation for the Adiponectin Paradox.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Therapeutic Potential ofParkinson's disease · 2021
    Review
  20. Review
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 4 institutions in 2 countries.

Masaaki WaragaiLaboratory for Parkinson's Disease, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Gilbert HoDepartment of Neurodegenerative Diseases, PCND Neuroscience Research Institute, Poway, CA, United States.
Yoshiki TakamatsuLaboratory for Parkinson's Disease, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Ryoko WadaLaboratory for Parkinson's Disease, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Shuei SugamaDepartment of Physiology, Nippon Medical School, Tokyo, Japan.
Takato TakenouchiInstitute of Agrobiological Sciences, National Agriculture and Food Research Organization, Tsukuba, Japan.
Eliezer MasliahDivision of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD, United States.
Makoto HashimotoLaboratory for Parkinson's Disease, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Tokyo Metropolitan Institute of Medical Science · JPNational Agriculture and Food Research Organization · JPNational Institute on Aging · USNippon Medical School · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adiponectin (APN) is a multi-functional adipokine which sensitizes the insulin signals, stimulates mitochondria biogenesis, and suppresses inflammation. By virtue of these beneficial properties, APN may protect against metabolic syndrome, including obesity and type II diabetes mellitus. Since these diseases are associated with hypoadiponectinemia, it is suggested that loss of function of APN might be involved. In contrast, despite beneficial properties for cardiovascular cells, APN is detrimental in circulatory diseases, including chronic heart failure (CHF) and chronic kidney disease (CKD). Notably, such an APN paradox might also be applicable to neurodegeneration. Although APN is neuroprotective in various experimental systems, APN was shown to be associated with the severity of amyloid accumulation and cognitive decline in a recent prospective cohort study in elderly. Furthermore, Alzheimer's disease (AD) was associated with hyperadiponectinemia in many studies. Moreover, APN was sequestered by phospho-tau into the neurofibrillary tangle in the postmortem AD brains. These results collectively indicate that APN might increase the risk of AD. In this context, the objective of the present study is to elucidate the mechanism of the APN paradox in AD. Hypothetically, APN might be involved in the stimulation of the amyloidogenic evolvability in reproductive stage, which may later manifest as AD by the antagonistic pleiotropy mechanism during aging. Given the accumulating evidence that AD and CHF are mechanistically overlapped, it is further proposed that the APN paradox of AD might be converged with those of other diseases, such as CHF and CKD.

Indexed as

AdiponectinAgingAlzheimer DiseaseAmyloidogenic ProteinsAnimalsBrainCognitive DysfunctionDisease Models, AnimalDisease ProgressionHumansMiceNerve DegenerationNeuronsNeuroprotectionAdiponectinAmyloidogenic Proteinsadiponectinadiponectin paradoxAlzheimer's disease (AD)antagonistic pleiotropychronic heart failure (CHF)evolvability

Identifiers

PMID32194507
PMCPMC7065259
OpenAlexW3009278150

What OpenQuestion holds

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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.