Evidence map›Paper›PMID 39516072›Full record

ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2025

From defense to disease: IFITM3 in immunity and Alzheimer's disease.

Zoe Kehs, Abigail C Cross, Yue-Ming Li

Abstract readReview
In one paragraph

Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Emerging approaches to bridging discovery science with clinical care in Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  8. Article
  9. Review
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

3 authors.

Zoe KehsChemical Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA; Programs of Pharmacology, Weill Graduate School of Medical Sciences of Cornell University, New York, NY, USA.
Abigail C CrossChemical Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA; Programs of Neuroscience, Weill Graduate School of Medical Sciences of Cornell University, New York, NY, USA.
Yue-Ming LiChemical Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA; Programs of Pharmacology, Weill Graduate School of Medical Sciences of Cornell University, New York, NY, USA. Electronic address: liy2@mskcc.org.

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Predoctoral Training in Pharmacological SciencesT32GM141949 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI Kristen Elizabeth Pleil · 2021 to 2026
$2.5M
NCI NIH HHS P30 CA008748NIGMS NIH HHS T32 GM141949
6 · The paper itself

Abstract

Innate immunity protein interferon induced transmembrane protein 3 (IFITM3) is a transmembrane protein that has a wide array of functions, including in viral infections, Alzheimer's Disease (AD), and cancer. As an interferon stimulated gene (ISG), IFITM3's expression is upregulated by type-I, II, and III interferons. Moreover, the antiviral activity of IFITM3 is modulated by post-translational modifications. IFITM3 functions in innate immunity to disrupt viral fusion and entry to the plasma membrane as well as prevent viral escape from endosomes. As a γ-secretase modulatory protein, IFITM3 distinctly modulates the processing of amyloid precursor protein (APP) to generate amyloid beta peptides (Aβ) and Notch1 cleavages. Increased IFITM3 expression, which can result from aging, cytokine activation, inflammation, and infection, can lead to an upregulation of γ-secretase for Aβ production that causes a risk of AD. Therefore, the prevention of IFITM3 upregulation has potential in the development of novel therapies for the treatment of AD.

Indexed as

Alzheimer DiseaseImmunity, InnateMembrane ProteinsRNA-Binding ProteinsAnimalsHumansIFITM3 protein, humanMembrane ProteinsRNA-Binding ProteinsAmyloidInfectionInflammationInnate immunityNeuroimmunologyγ-Secretase

Identifiers

PMID39516072
PMCPMC12047391

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.