Evidence map›Paper›PMID 30736297›Full record

ArticleInternational journal of molecular sciences2019

The Role of NOX4 in Parkinson's Disease with Dementia.

Dong-Hee Choi, In-Ae Choi, Cheol Soon Lee, Ji Hee Yun, Jongmin Lee

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

8 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. miR-204-3p/Nox4 Mediates Memory Deficits in a Mouse Model of Alzheimer's Disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Article
  5. Review
  6. Article
  7. Article
  8. 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

5 authors at 1 institution in 1 country.

Dong-Hee ChoiCenter for Neuroscience Research, Institute of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea. dchoi@kku.ac.kr.
In-Ae ChoiCenter for Neuroscience Research, Institute of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea. adia86@naver.com.
Cheol Soon LeeCenter for Neuroscience Research, Institute of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea. slaoa1428@naver.com.
Ji Hee YunCenter for Neuroscience Research, Institute of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea. bsea78@empas.com.
Jongmin LeeCenter for Neuroscience Research, Institute of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea. leej@kuh.ac.kr.ORCID 0000-0001-8718-0099
Konkuk University · KR

Funding

National Research Foundation of Korea NRF-2014R1A2A1A11050236National Research Foundation of Korea NRF-2016R1A5A2012284National Research Foundation of Korea NRF-2017R1A2B4004837
6 · The paper itself

Abstract

The neuropathology of Parkinson's disease with dementia (PDD) has been reported to involve heterogeneous and various disease mechanisms. Alpha-synuclein (α-syn) and amyloid beta (Aβ) pathology are associated with the cognitive status of PDD, and NADPH oxidase (NOX) is known to affect a variety of cognitive functions. We investigated the effects of NOX on cognitive impairment and on α-syn and Aβ expression and aggregation in PDD. In the 6-hydroxydopamine (6-OHDA)-injected mouse model, cognitive and motor function, and the levels of α-syn, Aβ, and oligomer A11 after inhibition of NOX4 expression in the hippocampal dentate gyrus (DG) were measured by the Morris water maze, novel object recognition, rotation, and rotarod tests, as well as immunoblotting and immunohistochemistry. After 6-OHDA administration, the death of nigrostriatal dopamine neurons and the expression of α-syn and NOX1 in the substantia nigra were increased, and phosphorylated α-syn, Aβ, oligomer A11, and NOX4 were upregulated in the hippocampus. 6-OHDA dose-dependent cognitive impairment was observed, and the increased cognitive impairment, Aβ expression, and oligomer A11 production in 6-OHDA-treated mice were suppressed by NOX4 knockdown in the hippocampal DG. Our results suggest that increased expression of NOX4 in the hippocampal DG in the 6-OHDA-treated mouse induces Aβ expression and oligomer A11 production, thereby reducing cognitive function.

Indexed as

AgedAged, 80 and overalpha-SynucleinAmyloid beta-PeptidesAnimalsBiomarkersCorpus StriatumDementiaDisease Models, AnimalGene Knockdown TechniquesHippocampusHumansMaleMiceMiddle AgedNADPH Oxidase 4alpha-SynucleinAmyloid beta-PeptidesBiomarkersNADPH Oxidase 4A11 oligomeralpha-synucleinamyloid betacognitive impairmenthippocampusNADPH oxidaseParkinson’s disease

Identifiers

PMID30736297
PMCPMC6386874
OpenAlexW2911349363

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.