Evidence map›Paper›PMID 31308793›Full record

ArticleExperimental neurobiology2019

The First Generation of iPSC Line from a Korean Alzheimer's Disease Patient Carrying APP-V715M Mutation Exhibits a Distinct Mitochondrial Dysfunction.

Ling Li, Jee Hoon Roh, Hee Jin Kim, Hyun Jung Park, Minchul Kim, Wonyoung Koh, Hyohoon Heo, Jong Wook Chang, Mahito Nakanishi, Taeyoung Yoon and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Experimental neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

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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

12 authors at 6 institutions in 2 countries.

Ling LiCHA Stem Cell Institute, Department of Biomedical Science, CHA University, Seongnam 13488, Korea.
Jee Hoon RohDepartment of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Hee Jin KimNeuroscience Center, Samsung Medical Center, Seoul 06351, Korea.
Hyun Jung ParkCHA Stem Cell Institute, Department of Biomedical Science, CHA University, Seongnam 13488, Korea.
Minchul KimCHA Stem Cell Institute, Department of Biomedical Science, CHA University, Seongnam 13488, Korea.
Wonyoung KohCHA Stem Cell Institute, Department of Biomedical Science, CHA University, Seongnam 13488, Korea.
Hyohoon HeoCHA Stem Cell Institute, Department of Biomedical Science, CHA University, Seongnam 13488, Korea.
Jong Wook ChangNeuroscience Center, Samsung Medical Center, Seoul 06351, Korea.
Mahito NakanishiResearch Center for Stem Cell Engineering, National Institute of Advanced Industrial Science and Technology (AIST), Ibaraki 305-8561, Japan.
Taeyoung YoonDong-A Socio R&D Center, Dong-A ST, Yongin 17073, Korea.
Duk L NaNeuroscience Center, Samsung Medical Center, Seoul 06351, Korea.
Jihwan SongCHA Stem Cell Institute, Department of Biomedical Science, CHA University, Seongnam 13488, Korea.
CHA University · KRSungkyunkwan University · KRDong-A ST (South Korea) · KRNational Institute of Advanced Industrial Science and Technology · JPSamsung Medical Center · KRUlsan College · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's Disease (AD) is a progressive neurodegenerative disease, which is pathologically defined by the accumulation of amyloid plaques and hyper-phosphorylated tau aggregates in the brain. Mitochondrial dysfunction is also a prominent feature in AD, and the extracellular Aβ and phosphorylated tau result in the impaired mitochondrial dynamics. In this study, we generated an induced pluripotent stem cell (iPSC) line from an AD patient with amyloid precursor protein (APP) mutation (Val715Met; APP-V715M) for the first time. We demonstrated that both extracellular and intracellular levels of Aβ were dramatically increased in the APP-V715M iPSC-derived neurons. Furthermore, the APP-V715M iPSC-derived neurons exhibited high expression levels of phosphorylated tau (AT8), which was also detected in the soma and neurites by immunocytochemistry. We next investigated mitochondrial dynamics in the iPSC-derived neurons using Mito-tracker, which showed a significant decrease of anterograde and retrograde velocity in the APP-V715M iPSC-derived neurons. We also found that as the Aβ and tau pathology accumulates, fusion-related protein Mfn1 was decreased, whereas fission-related protein DRP1 was increased in the APP-V715M iPSC-derived neurons, compared with the control group. Taken together, we established the first iPSC line derived from an AD patient carrying APP-V715M mutation and showed that this iPSC-derived neurons exhibited typical AD pathological features, including a distinct mitochondrial dysfunction.

Indexed as

Alzheimer's diseaseAmyloid betaAPPiPSCMitochondrial dysfunction

Identifiers

PMID31308793
PMCPMC6614069
OpenAlexW2954788058

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Registered trials

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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.