Evidence map›Paper›PMID 37669383›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2023

Nasal administration of anti-CD3 monoclonal antibody ameliorates disease in a mouse model of Alzheimer's disease.

Juliana R Lopes, Xiaoming Zhang, Julia Mayrink, Bruna K Tatematsu, Lydia Guo, Danielle S LeServe, Hadi Abou-El-Hassan, Felipe Rong, Maria J Dalton, Marilia G Oliveira and 5 more

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06868628 (A Phase 2a Study to Evaluate Microglial Activation, Safety, and Clinical Effects of Foralumab Nasal in Patients With Multiple System Atrophy), which is not on this map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.3field-weighted citation impact, top 7% 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.

NCT06868628 phase2recruitingnot on this mapstarted 2025, after this paper: background citation

A Phase 2a Study to Evaluate Microglial Activation, Safety, and Clinical Effects of Foralumab Nasal in Patients With Multiple System Atrophy (MSA)

TypeinterventionalSponsorTiziana Life Sciences LTDRan2025 to 2027Enrolled5ConditionsMultiple System AtrophyArmsForalumab Nasal
3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  7. Immune dysfunction in Alzheimer disease.Nature reviews. Neuroscience · 2026
    Review
  8. Article
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  14. Review
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  16. Immune modulation to treat Alzheimer's disease.Molecular neurodegeneration · 2025
    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

15 authors at 1 institution in 1 country.

Juliana R Lopes *Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.ORCID 0009-0009-6136-8830
Xiaoming Zhang *Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.ORCID 0000-0003-2654-3620
Julia MayrinkAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Bruna K TatematsuAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Lydia GuoAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.ORCID 0000-0002-6702-1223
Danielle S LeServeAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.ORCID 0009-0006-7020-9928
Hadi Abou-El-HassanAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.ORCID 0000-0002-2765-291X
Felipe RongAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.ORCID 0000-0002-2680-2381
Maria J DaltonAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.ORCID 0009-0005-7415-1885
Marilia G OliveiraAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Toby B LanserAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.ORCID 0000-0002-2250-6075
Lei LiuAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.ORCID 0000-0002-4604-4629
Oleg ButovskyAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Rafael M RezendeAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.ORCID 0000-0003-3998-8012
Howard L WeinerAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.ORCID 0000-0003-0203-9681
Brigham and Women's Hospital · US

Funding

Targeting CNS neuroinflammation in animal models of Alzheimer's diseaseR21AG063187 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI WEINER, HOWARD L · 2020 to 2020
$480k
NIA NIH HHS R21 AG063187
6 · The paper itself

Abstract

Emerging evidence suggests that dysregulation of neuroinflammation, particularly that orchestrated by microglia, plays a significant role in the pathogenesis of Alzheimer's disease (AD). Danger signals including dead neurons, dystrophic axons, phosphorylated tau, and amyloid plaques alter the functional phenotype of microglia from a homeostatic (M0) to a neurodegenerative or disease-associated phenotype, which in turn drives neuroinflammation and promotes disease. Thus, therapies that target microglia activation constitute a unique approach for treating AD. Here, we report that nasally administered anti-CD3 monoclonal antibody in the 3xTg AD mouse model reduced microglial activation and improved cognition independent of amyloid beta deposition. In addition, gene expression analysis demonstrated decreased oxidative stress, increased axogenesis and synaptic organization, and metabolic changes in the hippocampus and cortex of nasal anti-CD3 treated animals. The beneficial effect of nasal anti-CD3 was associated with the accumulation of T cells in the brain where they were in close contact with microglial cells. Taken together, our findings identify nasal anti-CD3 as a unique form of immunotherapy to treat Alzheimer's disease independent of amyloid beta targeting.

Indexed as

Alzheimer DiseaseAdministration, IntranasalAmyloid beta-PeptidesAnimalsAntibodies, MonoclonalDisease Models, AnimalMiceNeuroinflammatory DiseasesAmyloid beta-PeptidesAntibodies, Monoclonal3xTg micemicroglianasal anti-CD3T cells

Identifiers

PMID37669383
PMCPMC10500187
OpenAlexW4386452926

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.