Evidence map›Paper›PMID 32486466›Full record

ArticleInternational journal of molecular sciences2020

Human Neural Stem Cells Encoding ChAT Gene Restore Cognitive Function via Acetylcholine Synthesis, Aβ Elimination, and Neuroregeneration in APPswe/PS1dE9 Mice.

Dongsun Park, Ehn-Kyoung Choi, Tai-Hyoung Cho, Seong Soo Joo, Yun-Bae Kim

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

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  3. Oral Supplementation withNutrients · 2025
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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

5 authors at 4 institutions in 1 country.

Dongsun ParkDepartment of Biology Education, Korea National University of Education, Cheongju, Chungbuk 29173, Korea.
Ehn-Kyoung ChoiCentral Research Institute, Designed Cells Co., Ltd., Cheongju, Chungbuk 28576, Korea.
Tai-Hyoung ChoDepartment of Neurosurgery, Korea University College of Medicine, Korea University Anam Hospital, Seoul 02841, Korea.
Seong Soo JooDepartment of Marine Molecular Biotechnology, Gangneung-Wonju National University, Gangneung, Gangwon 25457, Korea.
Yun-Bae KimCentral Research Institute, Designed Cells Co., Ltd., Cheongju, Chungbuk 28576, Korea.ORCID 0000-0003-1340-041X
Chungbuk National University · KRGangneung–Wonju National University · KRKorea National University of Education · KRKorea University Medical Center · KR

Funding

National Research Foundation of Korea 2017R1A2A2A05069417
6 · The paper itself

Abstract

In Alzheimer disease (AD) patients, degeneration of the cholinergic system utilizing acetylcholine for memory acquisition is observed. Since AD therapy using acetylcholinesterase (AChE) inhibitors are only palliative for memory deficits without slowing or reversing disease progress, there is a need for effective therapies, and stem cell-based therapeutic approaches targeting AD should fulfill this requirement. We established a human neural stem cell (NSC) line encoding choline acetyltransferase (ChAT) gene, an acetylcholine-synthesizing enzyme. APPswe/PS1dE9 AD model mice transplanted with the F3.ChAT NSCs exhibited improved cognitive function and physical activity. Transplanted F3.ChAT NSCs in the AD mice differentiated into neurons and astrocytes, produced ChAT protein, increased the ACh level, and improved the learning and memory function. F3.ChAT cell transplantation reduced Aβ deposits by recovering microglial function; i.e., the down-regulation of β-secretase and inflammatory cytokines and up-regulation of Aβ-degrading enzyme neprilysin. F3.ChAT cells restored growth factors (GFs) and neurotrophic factors (NFs), and they induced the proliferation of NSCs in the host brain. These findings indicate that NSCs overexpressing ChAT can ameliorate complex cognitive and physical deficits of AD animals by releasing ACh, reducing Aβ deposit, and promoting neuroregeneration by the production of GFs/NFs. It is suggested that NSCs overexpressing ChAT could be a candidate for cell therapy in advanced AD therapy.

Indexed as

RegenerationAcetylcholineAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsAstrocytesBrainCell- and Tissue-Based TherapyCell ProliferationCholine O-AcetyltransferaseCognitionCognition DisordersHippocampusHumansMemory DisordersMiceAcetylcholineAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAPP protein, mouseCholine O-AcetyltransferaseNerve Growth FactorsPresenilin-1presenilin 1, mouseReceptors, CholinergicacetylcholineAlzheimer diseaseAβ depositioncholine acetyltransferasehuman neural stem cellneuroregeneration

Identifiers

PMID32486466
PMCPMC7313059
OpenAlexW3029586477

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.