Evidence map›Paper›PMID 26503303›Full record

ArticleScientific reports2015

High ω3-polyunsaturated fatty acids in fat-1 mice prevent streptozotocin-induced Purkinje cell degeneration through BDNF-mediated autophagy.

Dong Ho Bak, Enji Zhang, Min-Hee Yi, Do-Kyung Kim, Kyu Lim, Jwa-Jin Kim, Dong Woon Kim

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Nutraceuticals as Modulators of Autophagy: Relevance in Parkinson's Disease.International journal of molecular sciences · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Accumulation ofNeurology research international · 2017
    Article
  14. 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

7 authors at 3 institutions in 2 countries.

Dong Ho BakDepartment of Anatomy, College of Medicine, Konyang University of Korea, Daejeon, South Korea.
Enji ZhangDepartment of Anatomy, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, South Korea.
Min-Hee YiDepartment of Anatomy, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, South Korea.
Do-Kyung KimDepartment of Pharmacology, College of Medicine, Konyang University of Korea, Daejeon, South Korea.
Kyu LimDepartment of Biochemistry, Infection Signaling Network Research Center, Chungnam National University School of Medicine, Daejeon, South Korea.
Jwa-Jin KimDepartment of Anatomy, College of Medicine, Konyang University of Korea, Daejeon, South Korea.
Dong Woon KimDepartment of Anatomy, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, South Korea.
Chungnam National University · KRKonyang University · KRYanbian University Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of Purkinje cells has been implicated in the development of diabetic neuropathy, and this degeneration is characterized by impairment of autophagic processes. We evaluated whether fat-1 transgenic mice, a well-established animal model that endogenously synthesizes ω3 polyunsaturated fatty acids (ω3-PUFA), are protected from Purkinje cell degeneration in streptozotocin (STZ)-treated model with fat-1 mice. STZ-treated fat-1 mice did not develop hyperglycemia, motor deficits, or Purkinje cell loss. The expression of LC3 I, II, Beclin-1 and p62 were increased in the cerebellum of STZ-treated wild-type mice, and these expressions were more increased in STZ-treated fat-1 mice, but not of p62. Moreover, cerebellar Rab7, Cathepsin D, and ATP6E were increased in STZ-treated fat-1 mice. There was also increased BDNF expression in Purkinje cells without any changes in TrkB, and phosphorylation of Akt and CREB in the cerebellums of fat-1 mice. Collectively, these findings indicate that STZ-treated fat-1 mice were protected from Purkinje cell loss and exhibited increased BDNF signaling, enhancing autophagic flux activity in cerebellar Purkinje neurons. These processes may underlie Purkinje cell survival and may be potential therapeutic targets for treatment of motor deficits related to diabetic neuropathy.

Indexed as

AutophagyAnimalsBrain-Derived Neurotrophic FactorFatty Acids, Omega-3MicePurkinje CellsStreptozocinBrain-Derived Neurotrophic FactorFatty Acids, Omega-3Streptozocin

Identifiers

PMID26503303
PMCPMC4621527
OpenAlexW2403160513

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.