Evidence map›Paper›PMID 30611289›Full record

ArticleJournal of neuroinflammation2019

Peripheral adaptive immunity of the triple transgenic mouse model of Alzheimer's disease.

Isabelle St-Amour, Cristina R Bosoi, Isabelle Paré, Prenitha Mercy Ignatius Arokia Doss, Manu Rangachari, Sébastien S Hébert, Renée Bazin, Frédéric Calon

Abstract read
In one paragraph

Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

  1. Article
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  7. Causal relationships between peripheral immune cells and Alzheimer's disease: a two-sample Mendelian randomization study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Article
  8. Article
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  11. The effects of high plasma levels of AβImmunity & ageing : I & A · 2023
    Article
  12. Review
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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.

Isabelle St-AmourAxe Neurosciences, Centre de recherche du CHU de Québec-Université Laval, QC, Québec, Canada.
Cristina R BosoiAxe Neurosciences, Centre de recherche du CHU de Québec-Université Laval, QC, Québec, Canada.
Isabelle ParéMedical Affairs and Innovation, Héma-Québec, QC, Québec, Canada.
Prenitha Mercy Ignatius Arokia DossAxe Neurosciences, Centre de recherche du CHU de Québec-Université Laval, QC, Québec, Canada.
Manu RangachariAxe Neurosciences, Centre de recherche du CHU de Québec-Université Laval, QC, Québec, Canada.
Sébastien S HébertAxe Neurosciences, Centre de recherche du CHU de Québec-Université Laval, QC, Québec, Canada.
Renée BazinMedical Affairs and Innovation, Héma-Québec, QC, Québec, Canada.
Frédéric CalonAxe Neurosciences, Centre de recherche du CHU de Québec-Université Laval, QC, Québec, Canada. Frederic.Calon@crchudequebec.ulaval.ca.

Funding

Canadian Institute of Health Research ID0E4OAE13151Héma-Québec Foundation ISO-102447
6 · The paper itself

Abstract

backgroundImmunologic abnormalities have been described in peripheral blood and central nervous system of patients suffering from Alzheimer's disease (AD), yet their role in the pathogenesis still remains poorly defined. AIM AND

methodsWe used the triple transgenic mouse model (3xTg-AD) to reproduce Aβ (amyloid plaques) and tau (neurofibrillary tangles) neuropathologies. We analyzed important features of the adaptive immune system in serum, primary (bone marrow) as well as secondary (spleen) lymphoid organs of 12-month-old 3xTg-AD mice using flow cytometry and ELISPOT. We further investigated serum cytokines of 9- and 13-month-old 3xTg-AD mice using multiplex ELISA. Results were compared to age-matched non-transgenic controls (NTg).

resultsIn the bone marrow of 12-month-old 3xTg-AD mice, we detected decreased proportions of short-term reconstituting hematopoietic stem cells (0.58-fold, P = 0.0116), while lymphocyte, granulocyte, and monocyte populations remained unchanged. Our results also point to increased activation of both B and T lymphocytes. Indeed, we report elevated levels of plasma cells in bone marrow (1.3-fold, P = 0.0405) along with a 5.4-fold rise in serum IgG concentration (P < 0.0001) in 3xTg-AD animals. Furthermore, higher levels of interleukin (IL)-2 were detected in serum of 9- and 13-month-old 3xTg-AD mice (P = 0.0018). Along with increased concentrations of IL-17 (P = 0.0115) and granulocyte-macrophage colony-stimulating factor (P = 0.0085), these data support helper T lymphocyte activation with Th17 polarization.

conclusionCollectively, these results suggest that the 3xTg-AD model mimics modifications of the adaptive immunity changes previously observed in human AD patients and underscore the activation of both valuable and harmful pathways of immunity in AD.

Indexed as

Adaptive ImmunityAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsBone MarrowCell PolarityCytokinesGranulocytesHumansLymphocytesMiceMice, TransgenicMonocytesMutationNeurofibrillary TanglesAmyloid beta-PeptidesAmyloid beta-Protein PrecursorCytokinesPresenilin-1tau ProteinsAdaptive immune systemAlzheimer’s diseaseHematopoietic stem cellInflammationLymphocyte egressNeurodegenerative diseaseTh17

Identifiers

PMID30611289
PMCPMC6320637

What OpenQuestion holds

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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.