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Related Experiment Video

Updated: Jun 5, 2025

A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes
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Microglial lipid phosphatase SHIP1 limits complement-mediated synaptic pruning in the healthy developing hippocampus.

Alessandro Matera1, Anne-Claire Compagnion1, Chiara Pedicone2

  • 1Department of Biomedical Sciences, University of Lausanne, Lausanne, Switzerland.

Immunity
|December 10, 2024
PubMed
Summary
This summary is machine-generated.

SH2-containing inositol polyphosphate 5-phosphatase 1 (SHIP1) is crucial for healthy brain development and synaptic pruning by microglia. Early loss of microglial SHIP1 leads to lasting cognitive deficits and may increase Alzheimer

Keywords:
AD risk genesAlzheimer’s diseaseINPP5DSHIP1cognitive dysfunctioncomplementmicrogliasynaptic pruning

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Immunology

Background:

  • The INPP5D gene encodes the lipid phosphatase SHIP1, implicated in Alzheimer's disease risk.
  • The precise role of SHIP1 in microglial function and overall brain physiology remains largely unknown.
  • SHIP1 is observed to be enriched during early stages of healthy brain development.

Purpose of the Study:

  • To elucidate the function of SHIP1 in microglial cells during brain development.
  • To investigate the impact of microglial SHIP1 deficiency on synaptic remodeling and cognitive function.
  • To determine the long-term consequences of early-life microglial SHIP1 disruption.

Main Methods:

  • In vivo loss-of-function studies in mice with conditional microglial SHIP1 depletion.
  • Proteomic analysis to identify molecular changes in SHIP1-deficient microglia.
  • Utilized induced pluripotent stem cell (iPSC)-derived microglia for functional assays.

Main Results:

  • Conditional microglial SHIP1 deficiency led to increased complement-mediated synapse loss in the developing brain.
  • SHIP1-deficient microglia exhibited altered transcriptional profiles and aberrant synaptic pruning dependent on the complement system.
  • Early postnatal depletion of microglial SHIP1, but not later depletion, resulted in adult cognitive impairments.

Conclusions:

  • SHIP1 is essential for regulating microglia-mediated synapse remodeling during healthy brain development.
  • Disruption of SHIP1-dependent microglial function during early development has persistent behavioral consequences.
  • Impaired SHIP1 function in microglia may contribute to neurodegenerative disease vulnerability.