Evidence map›Paper›PMID 31036637›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

Pleiotropic neuroprotective effects of taxifolin in cerebral amyloid angiopathy.

Takayuki Inoue, Satoshi Saito, Masashi Tanaka, Hajime Yamakage, Toru Kusakabe, Akira Shimatsu, Masafumi Ihara, Noriko Satoh-Asahara

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  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 2 institutions in 1 country.

Takayuki InoueDepartment of Endocrinology, Metabolism, and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Fushimi-ku, 612-8555 Kyoto, Japan.
Satoshi SaitoDepartment of Neurology, National Cerebral and Cardiovascular Center, Suita, 565-8565 Osaka, Japan.
Masashi TanakaDepartment of Endocrinology, Metabolism, and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Fushimi-ku, 612-8555 Kyoto, Japan; masashi.7.tanaka@gmail.com.ORCID 0000-0003-0719-8972
Hajime YamakageDepartment of Endocrinology, Metabolism, and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Fushimi-ku, 612-8555 Kyoto, Japan.
Toru KusakabeDepartment of Endocrinology, Metabolism, and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Fushimi-ku, 612-8555 Kyoto, Japan.
Akira ShimatsuClinical Research Institute, National Hospital Organization Kyoto Medical Center, Fushimi-ku, 612-8555 Kyoto, Japan.
Masafumi IharaDepartment of Neurology, National Cerebral and Cardiovascular Center, Suita, 565-8565 Osaka, Japan.ORCID 0000-0002-7102-4048
Noriko Satoh-AsaharaDepartment of Endocrinology, Metabolism, and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Fushimi-ku, 612-8555 Kyoto, Japan.
Kyoto Medical Center · JPNational Cerebral and Cardiovascular Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebral amyloid angiopathy (CAA) results from amyloid-β deposition in the cerebrovasculature. It is frequently accompanied by Alzheimer's disease and causes dementia. We recently demonstrated that in a mouse model of CAA, taxifolin improved cerebral blood flow, promoted amyloid-β removal from the brain, and prevented cognitive dysfunction when administered orally. Here we showed that taxifolin inhibited the intracerebral production of amyloid-β through suppressing the ApoE-ERK1/2-amyloid-β precursor protein axis, despite the low permeability of the blood-brain barrier to taxifolin. Higher expression levels of triggering receptor expressed on myeloid cell 2 (TREM2) were associated with the exacerbation of inflammation in the brain. Taxifolin suppressed inflammation, alleviating the accumulation of TREM2-expressing cells in the brain. It also mitigated glutamate levels and oxidative tissue damage and reduced brain levels of active caspases, indicative of apoptotic cell death. Thus, the oral administration of taxifolin had intracerebral pleiotropic neuroprotective effects on CAA through suppressing amyloid-β production and beneficially modulating proinflammatory microglial phenotypes.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalBrainCerebral Amyloid AngiopathyDrug Evaluation, PreclinicalEndoplasmic Reticulum StressLymphatic VesselsMaleMiceMicrogliaQuercetinRandom AllocationAnti-Inflammatory Agents, Non-SteroidalQuercetintaxifolincerebral amyloid angiopathyneuroprotectiontaxifolintriggering receptor expressed on myeloid cell 2

Identifiers

PMID31036637
PMCPMC6525485
OpenAlexW2943645783

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.