Benjamin Singer
University of Michigan, MI·Neuroscience
People who survive sepsis, a life-threatening whole-body reaction to infection, carry more than a three-fold risk of new long-term problems with memory, thinking, and mood. Why some survivors develop this and others do not is poorly understood.
- Fields
Neuroscience
Microbiology & Immunology
Medicine & Clinical Research
- Topics
sepsis
amyloid beta
Alzheimer's disease
- Grants
- 1 known grant, through Dec 2026
What they work on
- Determine whether sepsis combined with presymptomatic amyloid deposition increases complement-driven neuroinflammation and synapse loss in 5xFAD mice, measuring microglial activation, engulfment of synapses, and synaptic transmission.
- Test whether behavioral deficits in 5xFAD sepsis survivors, including spatial memory, context discrimination, and motivation, depend on complement C3 signaling, using C3a receptor inhibition or inducible deletion of C3.
- Ask whether microglial engulfment of synapses after sepsis requires C3a signaling rather than microglial senescence, using a microfluidic cell culture platform to measure cytokine release and synaptosome phagocytosis.
- Establish whether sepsis-driven complement ligands and amyloid-induced complement receptors act together, by comparing amyloid-bearing and control mice that have survived a bacterial sepsis model.
More about the research
One candidate risk factor is common and usually silent: amyloid beta, the protein that accumulates in Alzheimer's disease, is already present in 20-50% of cognitively normal people over 60. This project asks whether that hidden amyloid makes the brain more vulnerable to injury after sepsis.
Why it matters
Cognitive and functional decline after sepsis is common and disabling, yet there is no way to predict or prevent it. By testing whether silent Alzheimer's-type amyloid pathology plus complement activation explains part of that decline, the work could identify a treatable pathway and help select which survivors might benefit from complement-targeting prevention in future clinical trials.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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University of Alabama at Birmingham, AL·Microbiology & Immunology
Determine how periodontitis regulates activation of microglia, the brain's resident immune cells, in Alzheimer's disease model mice, using three different experimental models of periodontal disease.
Dorothy Schafer
University of Massachusetts Chan Medical School, MA·Neuroscience
Determine whether microglia or other macrophages account for the reduced inflammation and improved remyelination seen in mice lacking UNC93B1, the chaperone eTLRs need, in acute and immune-mediated demyelination models.
Kim Dore
University of California-San Diego, CA·Neuroscience
Measure PSD-95 palmitoylation, the fatty tag that anchors this scaffold protein in synapses, across brain regions differently affected by Alzheimer's in APP/PS1 model mice and postmortem human brain samples.
The school
University of Michigan: 124 labs on PI Pages, $2.1B a year on research, 963 research doctorates a year.
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