Evidence map›Paper›PMID 27713140›Full record

ArticleOncotarget2016

Neuroprotective effects of CD4+CD25+Foxp3+ regulatory T cells in a 3xTg-AD Alzheimer's disease model.

Hyunjung Baek, Minsook Ye, Geun-Hyung Kang, Chanju Lee, Gihyun Lee, Da Bin Choi, Jaehoon Jung, Hyunseong Kim, Seonhwa Lee, Jin Su Kim and 4 more

Registry-linked trialOpen access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06489548 (Assessment of Foralumab Safety and Modulation of Microglial Activation Evaluated by PET Imaging in Patients With Early Symptomatic Alzheimer's Disease), which is not on this map. Cited by 113 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 3 pooled it
5.8field-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.

NCT06489548 phase2recruitingnot on this mapstarted 2025, after this paper: background citation

Assessment of Foralumab Safety and Modulation of Microglial Activation Evaluated by PET Imaging in Patients With Early Symptomatic Alzheimer's Disease

TypeinterventionalSponsorBrigham and Women's HospitalRan2025 to 2026Enrolled16ConditionsDementia, Alzheimers Disease, Mild Cognitive Impairment Due to Alzheimer's DiseaseArmsForalumab TZLS-401 50 µg, Foralumab TZLS-401 100 µg
3 · Its place in the literature

Who cites it

113 citing papers in PubMed, 3 syntheses or guidelines pooled it, 168 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Immune dysfunction in Alzheimer disease.Nature reviews. Neuroscience · 2026
    Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. CD28BMC neurology · 2025
    Article

53 more citing papers are in PubMed but not listed here.

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

14 authors at 4 institutions in 1 country.

Hyunjung BaekDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Minsook YeDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Geun-Hyung KangDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Chanju LeeDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Gihyun LeeDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Da Bin ChoiDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Jaehoon JungDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Hyunseong KimK-herb Research Center, Korea Institute of Oriental Medicine, Yuseongdae-ro, Yuseong-gu, Daejeon, Republic of Korea.
Seonhwa LeeDivision of RI Research, Korea Institute of Radiological & Medical Sciences University of Science & Technology, Gongneug-dong, Nowon-ku, Seoul, Republic of Korea.
Jin Su KimDivision of RI Research, Korea Institute of Radiological & Medical Sciences University of Science & Technology, Gongneug-dong, Nowon-ku, Seoul, Republic of Korea.
Hyun-Ju LeeAcupuncture and Meridian Science Research Center, College of Korean Medical Science Graduate School, Kyung Hee University, Seoul, Republic of Korea.
Insop ShimAcupuncture and Meridian Science Research Center, College of Korean Medical Science Graduate School, Kyung Hee University, Seoul, Republic of Korea.
Jun-Ho LeeDepartment of Biotechnology, Chonnam National University, Gwangju, Republic of Korea.
Hyunsu BaeDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Kyung Hee University · KRChonnam National University · KRKorea Institute of Radiological and Medical Sciences · KRKorea University of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease patients display neuropathological lesions, including the accumulation of amyloid-beta (Aβ) peptide and neurofibrillary tangles. Although the mechanisms causing the neurodegenerative process are largely unknown, increasing evidence highlights a critical role of immunity in the pathogenesis of Alzheimer's disease. In the present study, we investigated the role of regulatory T cells (Tregs) on Alzheimer's disease progression. First, we explored the effect of Tregs (CD4+CD25+ T cells) and Teffs (CD4+CD25- T cells) in an adoptive transfer model. Systemic transplantation of purified Tregs into 3xTg-AD mice improved cognitive function and reduced deposition of Aβ plaques. In contrast, adoptive transfer of Teffs diminished behavioral function and cytokine production. Next, we transiently depleted Treg population using an anti-CD25 antibody (PC61). Depletion of Tregs for four months resulted in a marked aggravation of the spatial learning deficits of six-month-old 3xTg-AD mice. Additionally, it resulted in decreasing glucose metabolism, as assessed by positron emission tomography (PET) with 18F-2 fluoro-2-deoxy-D-glucose ([F-18] FDG) neuroimaging. Importantly, the deposition of Aβ plaques and microglia/macrophage was increased in the hippocampal CA1 and CA3 regions of the Treg depleted 3xTg-AD compared to the vehicle-treated 3xTg-AD group. Our finding suggested that systemic Treg administration ameliorates disease progression and could be an effective Alzheimer's disease treatment.

Indexed as

Disease Models, AnimalAdoptive TransferAlzheimer DiseaseAnimalsForkhead Transcription FactorsGlucoseHippocampusHumansInterleukin-2 Receptor alpha SubunitLearning DisabilitiesMaleMemory DisordersMice, Inbred C57BLMice, TransgenicPositron-Emission TomographyT-Lymphocytes, RegulatoryForkhead Transcription FactorsFOXP3 protein, humanGlucoseInterleukin-2 Receptor alpha SubunitAlzheimer’s diseaseamyloid-beta (Aβ) pathologyImmune responseImmunityImmunology and Microbiology Sectionregulatory T cells (Treg)

Identifiers

PMID27713140
PMCPMC5342482
OpenAlexW2542427033

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.