Evidence map›Paper›PMID 22272619›Full record

ArticleCurrent Alzheimer research2012

Targeting phospho-Ser422 by active Tau Immunotherapy in the THYTau22 mouse model: a suitable therapeutic approach.

Laetitia Troquier, Raphaelle Caillierez, Sylvie Burnouf, Francisco J Fernandez-Gomez, Marie-Eve Grosjean, Nadege Zommer, Nicolas Sergeant, Susanna Schraen-Maschke, David Blum, Luc Buee

Abstract read
In one paragraph

Article in Current Alzheimer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
13.3field-weighted citation impact, top 1% 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

107 citing papers in PubMed, 186 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Immunotherapies: A Treasure Trove of Alzheimer's Disease.Current pharmaceutical biotechnology · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Tau and Alzheimer's disease: Past, present and future.Cytoskeleton (Hoboken, N.J.) · 2024
    Review
  12. Article
  13. Article
  14. Role of Tau protein in long COVID and potential therapeutic targets.Frontiers in cellular and infection microbiology · 2023
    Review
  15. Article
  16. Article
  17. Inhibition of Tau seeding by targeting Tau nucleation core within neurons with a single domain antibody fragment.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  18. Review
  19. Article
  20. Review

47 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

10 authors at 1 institution in 1 country.

Laetitia TroquierAlzheimer&Tauopathies, Centre de Recherches Jean-Pierre Aubert, Lille, France.
Raphaelle Caillierez
Sylvie Burnouf
Francisco J Fernandez-Gomez
Marie-Eve Grosjean
Nadege Zommer
Nicolas Sergeant
Susanna Schraen-Maschke
David Blum
Luc Buee
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent data indicate that Tau immunotherapy may be relevant for interfering with neurofibrillary degeneration in Alzheimer disease and related disorders referred to as Tauopathies. The key question for immunotherapy is the choice of the epitope to target. Abnormal phosphorylation is a well-described post-translational modification of Tau proteins and may be a good target. In the present study, we investigated the effects of active immunization against the pathological epitope phospho-Ser422 in the THY-Tau22 transgenic mouse model. Starting from 3-6 months of age, THY-Tau22 mice develop hippocampal neurofibrillary tangle-like inclusions and exhibit phosphorylation of Tau on several AD-relevant Tau epitopes. Three month-old THY-Tau22 mice were immunized with a peptide including the phosphoserine 422 residue while control mice received the adjuvant alone. A specific antibody response against the phospho-Ser422 epitope was observed. We noticed a decrease in insoluble Tau species (AT100- and pS422 immunoreactive) by both biochemical and immunohistochemical means correlated with a significant cognitive improvement using the Y-maze. This Tau immunotherapy may facilitate Tau clearance from the brain toward the periphery since, following immunization, an increase in Tau concentrations was observed in blood. Overall, the present work is, to our knowledge, the first one to demonstrate that active immunotherapy targeting a real pathological epitope such as phospho-Ser422 epitope is efficient. This immunotherapy allows for Tau clearance and improves cognitive deficits promoted by Tau pathology in a well-defined Tau transgenic model.

Indexed as

Age FactorsAlzheimer DiseaseAnimalsAntibodiesCognition DisordersDisease Models, AnimalEnzyme-Linked Immunosorbent AssayHippocampusHumansImmunotherapy, ActiveMaleMaze LearningMiceMice, Inbred C57BLMice, TransgenicMutationAntibodiesPeptidesSerinetau Proteins

Identifiers

PMID22272619
PMCPMC3637173
OpenAlexW2130365060

What OpenQuestion holds

Textmetadata
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.