Evidence map›Paper›PMID 26086962›Full record

ArticleCell death & disease2015

Neural stem cell transplantation at critical period improves learning and memory through restoring synaptic impairment in Alzheimer's disease mouse model.

J A Kim, S Ha, K Y Shin, S Kim, K J Lee, Y H Chong, K-A Chang, Y-H Suh

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

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 68 citations in OpenAlex.

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  5. Stem cell therapy offers new hope for the treatment of Alzheimer's disease.Frontiers in cell and developmental biology · 2025
    Review
  6. Proposed Mechanisms of Cell Therapy for Alzheimer's Disease.International journal of molecular sciences · 2024
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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

8 authors at 4 institutions in 1 country.

J A KimDepartment of Pharmacology, College of Medicine, Neuroscience Research Institute, MRC, Seoul National University, Seoul, 110-799, Korea.
S HaDepartment of Pharmacology, College of Medicine, Neuroscience Research Institute, Gachon University, Incheon, 405-760, Korea.
K Y ShinDepartment of Pharmacology, College of Medicine, Neuroscience Research Institute, MRC, Seoul National University, Seoul, 110-799, Korea.
S KimDepartment of Pharmacology, College of Medicine, Neuroscience Research Institute, Gachon University, Incheon, 405-760, Korea.
K J LeeSynaptic Circuit Plasticity Laboratory, Department of Structure & Function of Neural Network, Korea Brain Research Institute, 61 Cheomdan-ro, Dong-gu, Daegu 701-300, Korea.
Y H ChongDivision of Molecular Biology and Neuroscience, Department of Microbiology, School of Medicine, Ewha Medical Research Institute, Ewha Womans University, Seoul, 158-710, Korea.
K-A ChangDepartment of Pharmacology, College of Medicine, Neuroscience Research Institute, Gachon University, Incheon, 405-760, Korea.
Y-H Suh1] Department of Pharmacology, College of Medicine, Neuroscience Research Institute, MRC, Seoul National University, Seoul, 110-799, Korea [2] Synaptic Circuit Plasticity Laboratory, Department of Structure & Function of Neural Network, Korea Brain Research Institute, 61 Cheomdan-ro, Dong-gu, Daegu 701-300, Korea.
Gachon University · KRKorea Brain Research Institute · KRSeoul National University · KREwha Womans University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by neuronal loss in several regions of the brain. Recent studies have suggested that stem cell transplantation could serve as a potential therapeutic strategy to halt or ameliorate the inexorable disease progression. However, the optimal stage of the disease for stem cell transplantation to have a therapeutic effect has yet to be determined. Here, we demonstrated that transplantation of neural stem cells into 12-month-old Tg2576 brains markedly improved both cognitive impairments and neuropathological features by reducing β-amyloid processing and upregulating clearance of β-amyloid, secretion of anti-inflammatory cytokines, endogenous neurogenesis, as well as synapse formation. In contrast, the stem cell transplantation did not recover cognitive dysfunction and β-amyloid neuropathology in Tg2576 mice aged 15 months when the memory loss is manifest. Overall, this study underscores that stem cell therapy at optimal time frame is crucial to obtain maximal therapeutic effects that can restore functional deficits or stop the progression of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainCell- and Tissue-Based TherapyCells, CulturedCognition DisordersCytokinesDisease Models, AnimalMaze LearningMemoryMemory DisordersMiceMice, Inbred C57BLNeural Stem CellsNeurogenesisAmyloid beta-PeptidesCytokines

Identifiers

PMID26086962
PMCPMC4669825
OpenAlexW898411137

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.