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Related Concept Videos

TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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Updated: Feb 28, 2026

Immunofluorescence Staining Using IBA1 and TMEM119 for Microglial Density, Morphology and Peripheral Myeloid Cell Infiltration Analysis in Mouse Brain
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Impaired TGFβ Signaling in Plaque-Associated Microglia.

Oliver Krzyzan1,2, Angela Kuhla3,4, Björn Spittau5

  • 1Institute of Anatomy, Rostock Medical Centre, Rostock University, 18057 Rostock, Germany.

Biomolecules
|February 27, 2026
PubMed
Summary
This summary is machine-generated.

This study reveals that Alzheimer's disease (AD) in mice disrupts microglial cell shape and transforming growth factor beta (TGF-β) signaling. These changes in glial cells and TGF-β pathways may contribute to AD development.

Keywords:
3D morphologyAPP/PS1Alzheimer’s diseaseSMAD proteinsTGF-βconfocal microscopymicroglianeuroinflammation

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Aging and Alzheimer's disease (AD) are linked to significant alterations in glial cell structure and function.
  • Microglia, the brain's immune cells, and transforming growth factor beta (TGF-β) signaling are implicated in AD pathogenesis.

Purpose of the Study:

  • To investigate the three-dimensional morphology of microglia.
  • To examine the intracellular localization of phosphorylated SMAD proteins, key effectors of TGF-β signaling.
  • To analyze these factors in the amyloid precursor protein and presenilin-1 (APP/PS1) transgenic mouse model of AD.

Main Methods:

  • Utilized confocal microscopy for high-resolution imaging of glial cells.
  • Employed Simple Neurite Tracer software for quantitative analysis of cell morphology.
  • Performed immunofluorescence staining to detect pSMAD2 protein localization in microglia.

Main Results:

  • Observed significant alterations in the three-dimensional morphology of microglia in APP/PS1 mice compared to wild-type controls.
  • Found altered intracellular distribution of phosphorylated SMAD2 (pSMAD2) in microglia.
  • These findings suggest impaired canonical TGF-β signaling in the AD mouse model.

Conclusions:

  • The study demonstrates disturbed glial cell morphology in the APP/PS1 mouse model.
  • Dysfunctional TGF-β signaling cascade was identified in microglia within the AD model.
  • These cellular and signaling disturbances highlight a potential role in Alzheimer's disease pathogenesis.