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Innate immune crosstalk in ALS/FTD pathogenesis.

Xiaoqiu Shu1, Xinyuan Yu1, Pinglong Xu1,2

  • 1Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, and Life Sciences Institute, Zhejiang University, Hangzhou, 310058, China.

Cell Insight
|June 26, 2026
PubMed
Summary
This summary is machine-generated.

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) involve innate immune pathways like cGAS-STING and NLRP3 inflammasomes. Understanding this immune network is key for new therapies targeting neuroinflammation.

Keywords:
Amyotrophic lateral sclerosisFrontotemporal dementiaMicrogliaNLRP3 inflammasomeNeuroinflammationTREM2cGAS-STING

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Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
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Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Published on: December 26, 2016

Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are neurodegenerative diseases characterized by protein aggregation, impaired proteostasis, and neuroinflammation.
  • Innate immune activation is increasingly recognized as a driver of ALS/FTD progression, not just a response to neuronal damage.

Purpose of the Study:

  • To review how genetic lesions and protein aggregates in ALS/FTD engage innate immune pathways.
  • To explore the crosstalk among these immune pathways and its implications for disease progression.

Main Methods:

  • Literature review of studies on ALS/FTD genetics, proteinopathies, and innate immunity.
  • Analysis of the roles of cGAS-STING, NLRP3 inflammasomes, and TREM2-DAP12 signaling in ALS/FTD pathogenesis.

Main Results:

  • ALS/FTD-associated genetic factors and protein aggregates (TDP-43, SOD1, FUS, dipeptide repeats) activate cGAS-STING, NLRP3 inflammasomes, and TREM2-DAP12 pathways.
  • Crosstalk between cGAS-STING and NLRP3 amplifies inflammation; NLRP3-mediated TREM2 shedding may hinder microglial functions.

Conclusions:

  • The interconnected innate immune network in ALS/FTD contributes to disease progression.
  • Targeting this immune network offers potential for subtype definition, biomarker discovery, and combinatorial therapeutic strategies to modulate neuroinflammation and preserve microglial function.