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Assessing Aβ-independent effects of Module 42 on immune function in vitro.

Ishita Ajith1,2, Souvika Bakshi1, Emma Mead1,3

  • 1Centre for Medicines Discovery, Oxford, UK.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|February 25, 2026
PubMed
Summary

Module 42 (M42) proteins, linked to Alzheimer's disease (AD), impact immune cell function. Midkine (MDK) and TMEFF2 ectodomain altered phagocytosis and calcium signaling, suggesting a role in AD immunity beyond amyloid pathology.

Keywords:
Alzheimer's diseaseM42 proteinsimmune functionmatrisome

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Area of Science:

  • Neuroscience
  • Immunology
  • Proteomics

Background:

  • A novel protein network, Module 42 (M42), was identified in post-mortem human brains and is strongly correlated with Alzheimer's disease (AD) pathology.
  • M42 consists of 32 transmembrane and extracellular matrix proteins, including amyloid precursor protein (APP) and apolipoprotein E (apoE), implicated in amyloid beta (Aβ) pathology.

Purpose of the Study:

  • To systematically evaluate the Aβ-independent effects of M42 proteins on immune cell function in vitro.
  • To investigate the specific roles of M42 components in modulating immune responses relevant to AD.

Main Methods:

  • Recombinant M42 proteins were expressed and purified.
  • Human induced pluripotent stem cell-derived macrophages were treated with M42 proteins.
  • Assays assessed phagocytosis, intracellular calcium (Ca2+) signaling, and cell viability.

Main Results:

  • Midkine (MDK) reduced phagocytosis, while the ectodomain of Transmembrane protein with EGF-like and two follistatin-like domains 2 (TMEFF2) increased it.
  • Both MDK and TMEFF2 ectodomain promoted intracellular Ca2+ signaling.
  • TMEFF2 ectodomain suppressed Syk kinase activity; no M42 proteins affected cell viability.

Conclusions:

  • M42 proteins play a role in regulating immune functions independently of Aβ pathology.
  • These findings suggest M42 contributes to AD pathogenesis through modulation of immune responses.