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Progranulin Deficiency Promotes Circuit-Specific Synaptic Pruning by Microglia via Complement Activation.

Hansen Lui¹, Jiasheng Zhang¹, Stefanie R Makinson²

¹Department of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.

|April 27, 2016

Summary

This summary is machine-generated.

Progranulin deficiency in mice causes age-dependent microglial activation, leading to synaptic loss and obsessive-compulsive behaviors. Suppressing complement C1qa mitigates these neurodegenerative effects.

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Area of Science:

Neuroscience
Immunology
Genetics

Background:

Microglia are crucial for brain homeostasis, but their role in neurodegeneration is debated.
Progranulin (Grn) deficiency is linked to frontotemporal dementia (FTD), but the underlying mechanisms are unclear.

Purpose of the Study:

To investigate the role of progranulin deficiency in microglial activation and neurodegeneration.
To elucidate the mechanisms by which Grn deficiency impacts brain function and behavior.

Main Methods:

Transcriptome profiling of microglia from Grn-deficient mice.
Analysis of microglial infiltration, synaptic pruning, and thalamocortical circuit activity.
Genetic deletion of C1qa to assess its impact on Grn(-/-) phenotypes.

Main Results:

Grn deficiency caused age-dependent upregulation of lysosomal and immune genes in microglia.
Grn(-/-) mice exhibited increased synaptic pruning, thalamocortical hyperexcitability, and OCD-like behaviors.
C1qa deletion reduced synaptic pruning, mitigated neurodegeneration, and improved survival in Grn(-/-) mice.

Conclusions:

Progranulin normally suppresses aberrant microglial activation during aging.
Complement activation and microglia-mediated synaptic pruning are key drivers of neurodegeneration in Grn deficiency.
Targeting microglial complement pathways may offer therapeutic strategies for FTD and related disorders.