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Peripheral immune profiling in frontotemporal dementia.

Nazaret Gamez1, Abdulmunaim M Eid1, Belen Pascual1

  • 1Stanley H. Appel Department of Neurology, Houston Methodist Neurological Institute, Houston, TX 77030, USA.

Brain Communications
|April 2, 2026
PubMed
Summary
This summary is machine-generated.

Frontotemporal dementia (FTD) involves immune system dysfunction, with compromised regulatory T cells and increased inflammatory markers. This study reveals peripheral immune dysregulation in FTD patients, suggesting potential therapeutic targets.

Keywords:
Tregscytokinesfrontotemporal dementiaimmune systeminflammation

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Area of Science:

  • Neuroimmunology
  • Immunology
  • Neurology

Background:

  • Frontotemporal dementia (FTD) is a heterogeneous neurodegenerative disorder with subtypes including behavioral variant FTD, and semantic and non-fluent primary progressive aphasia.
  • Neuroinflammation is increasingly recognized as a shared pathogenic mechanism in FTD, yet the role of the peripheral immune system remains unclear.
  • Understanding peripheral immune system alterations in FTD is crucial for identifying novel diagnostic and therapeutic strategies.

Purpose of the Study:

  • To investigate the immunophenotypes of peripheral immune cell populations in individuals with FTD compared to healthy controls.
  • To assess the functional status of regulatory T cells and the immune-related transcriptomic profile of monocytes in FTD.
  • To quantify plasma levels of inflammatory cytokines and chemokines in FTD patients.

Main Methods:

  • Blood samples from 27 FTD patients (7 bvFTD, 10 nfvPPA, 10 svPPA) and 25 healthy controls were analyzed using multicolour flow cytometry.
  • Regulatory T cell function was assessed by co-culture assays measuring proliferation.
  • Monocyte transcriptomic profiling utilized the NanoString Human Inflammation Panel, and plasma cytokine/chemokine levels were quantified via Olink® Target 48 Cytokine panel.

Main Results:

  • Regulatory T cells from FTD individuals exhibited significantly compromised suppressive function on responder T cell proliferation compared to controls (P < 0.05).
  • FTD monocytes showed dysregulation in 153 immune-related genes, enriched in pathways like chemokine signaling and interferon-gamma response.
  • FTD patients displayed significantly elevated plasma levels of pro-inflammatory cytokine TNFa and chemokines CXCL10, CCL3, CCL19, CSF1, and CXCL12 compared to controls (P < 0.05 to P < 0.01).

Conclusions:

  • This study provides the first evidence of compromised immunomodulatory function of regulatory T cells in FTD.
  • Peripheral immune dysregulation in FTD includes altered monocyte gene expression and elevated plasma inflammatory mediators.
  • These findings highlight the potential of targeting regulatory T cells and modulating inflammation for FTD therapeutics.