Evidence map›Paper›PMID 29335844›Full record

ArticleMolecular neurobiology2018

The Adiponectin Homolog Osmotin Enhances Neurite Outgrowth and Synaptic Complexity via AdipoR1/NgR1 Signaling in Alzheimer's Disease.

Gwangho Yoon, Shahid Ali Shah, Tahir Ali, Myeong Ok Kim

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  10. Antioxidant and Anti-Inflammatory Effects ofAntioxidants (Basel, Switzerland) · 2020
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  18. The Role of KLFFrontiers in cellular neuroscience · 2018
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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

4 authors at 1 institution in 1 country.

Gwangho YoonDivision of Life Science and Applied Life Science (BK 21 plus), College of Natural Sciences, Gyeongsang National University, Jinju, 52828, South Korea.
Shahid Ali ShahDivision of Life Science and Applied Life Science (BK 21 plus), College of Natural Sciences, Gyeongsang National University, Jinju, 52828, South Korea.
Tahir AliDivision of Life Science and Applied Life Science (BK 21 plus), College of Natural Sciences, Gyeongsang National University, Jinju, 52828, South Korea.
Myeong Ok KimDivision of Life Science and Applied Life Science (BK 21 plus), College of Natural Sciences, Gyeongsang National University, Jinju, 52828, South Korea. mokim@gnu.ac.kr.
Gyeongsang National University · KR

Funding

National Research Foundation of Korea NRF-2016M3C7A1904391
6 · The paper itself

Abstract

Alzheimer's disease is a major neurodegenerative disease characterized by memory loss and cognitive deficits. Recently, we reported that osmotin, which is a homolog of adiponectin, improved long-term potentiation and cognitive functions in Alzheimer's disease mice. Several lines of evidence have suggested that Nogo-A and the Nogo-66 receptor 1 (NgR1), which form a complex that inhibits long-term potentiation and cognitive function, might be associated with the adiponectin receptor 1 (AdipoR1), which is a receptor for osmotin. Here, we explore whether osmotin's effects on long-term potentiation and memory function are associated with NgR1 signaling via AdipoR1 in Alzheimer's disease. Osmotin reduced the expression of NgR1 without affecting Nogo-A expression. Furthermore, osmotin inhibited NgR1 signaling by prohibiting the formation of the Nogo-A and NgR1 ligand-receptor complex, resulting in enhanced neurite outgrowth; these effects disappeared in the presence of AdipoR1 interference. In addition, osmotin increased the expression of the pre- and postsynaptic markers synaptophysin and PSD-95, as well as the activation of the memory-associated markers AMPA receptor and CREB; these effects occurred in an AdipoR1- and NgR1-dependent manner. Osmotin was also found to enhance dendritic complexity and spine density in the hippocampal region of Alzheimer's disease mouse brains. These results suggest that osmotin can enhance neurite outgrowth and synaptic complexity through AdipoR1 and NgR1 signaling, implying that osmotin might be an effective therapeutic agent for Alzheimer's disease and that AdipoR1 might be a crucial therapeutic target for neurodegenerative diseases such as Alzheimer's.

Indexed as

Signal TransductionAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBiomarkersBrainCell Line, TumorDisease Models, AnimalHumansMaleMemoryMice, Inbred C57BLMice, TransgenicNeuronal OutgrowthNogo ProteinsNogo Receptor 1Amyloid beta-PeptidesBiomarkersNogo ProteinsNogo Receptor 1osmotin protein, Nicotiana tabacumPlant ProteinsReceptors, AdiponectinRNA, MessengerAdiponectin receptor 1Alzheimer’s diseaseNeurite outgrowthNogo-66 receptor 1OsmotinSynaptic complexity

Identifiers

PMID29335844
OpenAlexW2783255908

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.