Evidence map›Paper›PMID 24412277›Full record

ReviewBiochemical pharmacology2014

Immunotherapy for Alzheimer's disease.

Thomas Wisniewski, Fernando Goñi

Abstract readReview
In one paragraph

Review in Biochemical pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
9.9field-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

58 citing papers in PubMed, 101 citations in OpenAlex.

  1. Review
  2. Alzheimer disease: Amyloid peptide controversies and challenges of anti-Aβ immunotherapy.The Journal of pharmacology and experimental therapeutics · 2025
    Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. The Overlap Index as a Means of Evaluating Early Tau PET Signal Reliability.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2022
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Immunotherapies Targeting α-Synuclein in Parkinson Disease.Federal practitioner : for the health care professionals of the VA, DoD, and PHS · 2020
    Article
  16. Review
  17. Article
  18. Article
  19. Nanoliposomes as a Therapeutic Tool for Alzheimer's Disease.Frontiers in synaptic neuroscience · 2020
    Review
  20. Article
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

2 authors at 1 institution in 1 country.

Thomas WisniewskiDepartments of Neurology, New York University School of Medicine, Alexandria ERSP, 450 East 29th Street, New York, NY 10016, United States; Departments of Pathology, New York University School of Medicine, Alexandria ERSP, 450 East 29th Street, New York, NY 10016, United States; Departments of Psychiatry, New York University School of Medicine, Alexandria ERSP, 450 East 29th Street, New York, NY 10016, United States. Electronic address: thomas.wisniewski@nyumc.org.
Fernando GoñiDepartments of Neurology, New York University School of Medicine, Alexandria ERSP, 450 East 29th Street, New York, NY 10016, United States.
New York University · US

Funding

PSYCHOSOCIAL COREP30AG008051 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SHAO, YONGZHAO · 1990 to 2019
$36.1M
Detection and Clearance of AD LesionsR01AG020245 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WISNIEWSKI, THOMAS M · 2002 to 2016
$4.7M
Therapeutic Targeting of Abnormal Conformation in Neurodegenerative DiseaseR01NS073502 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WISNIEWSKI, THOMAS M · 2010 to 2019
$3.7M
NIA NIH HHS AG08051NIA NIH HHS AG20245NIA NIH HHS P30 AG008051NIA NIH HHS R01 AG020245NINDS NIH HHS NS073502NINDS NIH HHS R01 NS073502
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common cause of dementia worldwide. In AD the normal soluble amyloid β (sAβ) peptide is converted into oligomeric/fibrillar Aβ. The oligomeric forms of Aβ are thought to be the most toxic, while fibrillar Aβ becomes deposited as amyloid plaques and congophilic angiopathy, which serve as neuropathological markers of the disease. In addition the accumulation of abnormally phosphorylated tau as soluble toxic oligomers and as neurofibrillary tangles is a critical part of the pathology. Numerous therapeutic interventions are under investigation to prevent and treat AD. Among the more exciting and advanced of these approaches is vaccination. Active and passive Immunotherapy targeting only Aβ has been successful in many AD model animal trials; however, the more limited human data has shown much less benefit so far, with encephalitis occurring in a minority of patients treated with active immunization and vasogenic edema or amyloid-related imaging abnormalities (ARIA) being a complication in some passive immunization trials. Therapeutic intervention targeting only tau has been tested only in mouse models; and no approaches targeting both pathologies concurrently has been attempted, until very recently. The immune approaches tried so far were targeting a self-protein, albeit in an abnormal conformation; however, effective enhanced clearance of the disease associated conformer has to be balanced with the potential risk of stimulating excessive toxic inflammation. The design of future more effective immunomodulatory approaches will need to target all aspects of AD pathology, as well as specifically targeting pathological oligomeric conformers, without the use of any self-antigen.

Indexed as

Immunization, PassiveImmunotherapy, ActiveAlzheimer DiseaseAmyloid beta-PeptidesHumansAmyloid beta-PeptidesAlzheimer's diseaseAmyloid βImmunomodulationTauTransgenic miceVaccination

Identifiers

PMID24412277
PMCPMC3972315
OpenAlexW2036272830

What OpenQuestion holds

Textmetadata
LicenceTDM
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.