Evidence map›Paper›PMID 33786807›Full record

ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2021

Ferulic Acid Ameliorates Alzheimer's Disease-like Pathology and Repairs Cognitive Decline by Preventing Capillary Hypofunction in APP/PS1 Mice.

Ni-Ya Wang, Jin-Nan Li, Wei-Lin Liu, Qi Huang, Wen-Xing Li, Ya-Hong Tan, Fang Liu, Zi-Hua Song, Meng-Yue Wang, Ning Xie and 8 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Inhibiting CaNature neuroscience · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Research progress of natural products and their derivatives against Alzheimer's disease.Journal of enzyme inhibition and medicinal chemistry · 2023
    Review
  18. Article
  19. 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

18 authors at 7 institutions in 2 countries.

Ni-Ya Wang *CAS Key Laboratory of Animal Models and Human Disease Mechanisms, and KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China.
Jin-Nan Li *CAS Key Laboratory of Animal Models and Human Disease Mechanisms, and KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China.
Wei-Lin Liu *The Academy of Rehabilitation Industry, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, China.
Qi Huang *Key Laboratory of Nuclear Analysis Techniques, Institute of High Energy Physics, the Chinese Academy of Sciences, Beijing, 100049, China.
Wen-Xing Li *CAS Key Laboratory of Animal Models and Human Disease Mechanisms, and KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China.
Ya-Hong TanCAS Key Laboratory of Animal Models and Human Disease Mechanisms, and KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China.
Fang LiuCAS Key Laboratory of Animal Models and Human Disease Mechanisms, and KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China.
Zi-Hua SongCAS Key Laboratory of Brain Function and Disease, Hefei National Laboratory for Physical Sciences At the Microscale, University of Science and Technology of China, Hefei, 230027, China.
Meng-Yue WangState Key Laboratory of Innovative Natural Drugs and Traditional Chinese Medicine Injections, Qingfeng Pharmaceutical Corporations, Ganzhou, 341000, China.
Ning XieState Key Laboratory of Innovative Natural Drugs and Traditional Chinese Medicine Injections, Qingfeng Pharmaceutical Corporations, Ganzhou, 341000, China.
Rong-Rong MaoCAS Key Laboratory of Animal Models and Human Disease Mechanisms, and KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China.
Ping GanCAS Key Laboratory of Animal Models and Human Disease Mechanisms, and KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China.
Yu-Qiang DingState Key Laboratory of Medical Neurobiology and MOE Frontiers Centre for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, 200032, China.
Zhi ZhangCAS Key Laboratory of Brain Function and Disease, Hefei National Laboratory for Physical Sciences At the Microscale, University of Science and Technology of China, Hefei, 230027, China.
Bao-Ci ShanKey Laboratory of Nuclear Analysis Techniques, Institute of High Energy Physics, the Chinese Academy of Sciences, Beijing, 100049, China. shanbc@ihep.ac.cn.
Li-Dian ChenThe Academy of Rehabilitation Industry, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, China. 1984010@fjtcm.edu.cn.
Qi-Xin ZhouCAS Key Laboratory of Animal Models and Human Disease Mechanisms, and KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China. qixin_zhou@vip.126.com.
Lin XuCAS Key Laboratory of Animal Models and Human Disease Mechanisms, and KIZ-SU Joint Laboratory of Animal Model and Drug Development, and Laboratory of Learning and Memory, Kunming Institute of Zoology, the Chinese Academy of Sciences, Kunming, 650223, China. lxu@vip.163.com.ORCID http://orcid.org/0000-0002-2710-3507
Kunming Institute of Zoology · CNChinese Academy of Sciences · CNFujian University of Traditional Chinese Medicine · CNUniversity of Science and Technology of China · CNCentral South University · CNFudan University · CNKunming Institute of Botany · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brain capillaries are crucial for cognitive functions by supplying oxygen and other nutrients to and removing metabolic wastes from the brain. Recent studies have demonstrated that constriction of brain capillaries is triggered by beta-amyloid (Aβ) oligomers via endothelin-1 (ET1)-mediated action on the ET1 receptor A (ETRA), potentially exacerbating Aβ plaque deposition, the primary pathophysiology of Alzheimer's disease (AD). However, direct evidence is still lacking whether changes in brain capillaries are causally involved in the pathophysiology of AD. Using APP/PS1 mouse model of AD (AD mice) relative to age-matched negative littermates, we identified that reductions of density and diameter of hippocampal capillaries occurred from 4 to 7 months old while Aβ plaque deposition and spatial memory deficit developed at 7 months old. Notably, the injection of ET1 into the hippocampus induced early Aβ plaque deposition at 5 months old in AD mice. Conversely, treatment of ferulic acid against the ETRA to counteract the ET1-mediated vasoconstriction for 30 days prevented reductions of density and diameter of hippocampal capillaries as well as ameliorated Aβ plaque deposition and spatial memory deficit at 7 months old in AD mice. Thus, these data suggest that reductions of density and diameter of hippocampal capillaries are crucial for initiating Aβ plaque deposition and spatial memory deficit at the early stages, implicating the development of new therapies for halting or curing memory decline in AD.

Indexed as

Amyloid beta-Protein PrecursorPresenilin-1Alzheimer DiseaseAnimalsAnti-Inflammatory Agents, Non-SteroidalCapillariesCognitive DysfunctionCoumaric AcidsHippocampusInjections, IntraventricularMaleMiceMice, Inbred C57BLMice, TransgenicAmyloid beta-Protein PrecursorAnti-Inflammatory Agents, Non-SteroidalCoumaric Acidsferulic acidPresenilin-1Alzheimer’s diseaseAPP/PS1 mouseAβ plaqueEndothelin-1Ferulic acid (FA)Hippocampus

Identifiers

PMID33786807
PMCPMC8423929
OpenAlexW3145007379

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.