Stanley Stevens
University of South Florida, FL·Neuroscience
Alcohol use disorder (AUD) damages many organs, including the brain. A key driver of this harm is the brain's immune response, led partly by microglia, the brain's resident immune cells.
- Fields
Neuroscience
Pharmacology
Biochemistry
- Topics
alcohol use disorder
microglia
neuroimmune response
- Grants
- 1 known grant, through Jul 2027
What they work on
- Generate and characterize human microglia derived from induced pluripotent stem cells (iPSCs) carrying mutant MetRS, the enzyme needed for BONCAT protein labeling, and measure their reactivity to alcohol in vitro.
- Characterize the human microglial response to alcohol in vivo using Chimera-BONCAT, a chimeric mouse whose brain contains engineered human microglia that label their own newly made proteins.
- Selectively enrich proteins from human microglia in the chimeric mouse brain after alcohol exposure and profile them with proteomics to map alcohol-induced changes in these cells.
More about the research
Microglia react to alcohol in many different ways depending on context, but the full molecular picture of these reactions is unknown. Most studies also rely on rodent microglia, which may not reflect what happens in people.
Why it matters
By capturing how human brain immune cells respond to alcohol inside a living brain, this model may yield findings that apply to people better than findings from standard rodent models. The work could improve understanding of how alcohol use disorder harms the human brain. It may also point toward neuroimmune processes worth targeting in future research.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Henry Kranzler
University of Pennsylvania, PA·Genetics
Map alcohol-linked GWAS variants to the genes they control by combining ATAC-seq (open DNA maps) and Capture C (maps of DNA looping) data from iPSC-derived cortical, dopaminergic and other neurons.
Tae-Wan Kim
Columbia University, NY·Neuroscience
Determine how the neuronal signal SEMA3A promotes β-amyloid uptake and a disease-associated microglia gene profile in human iPSC-derived microglia (iMGLs), independently of the TREM2 receptor.
Giuseppina Tesco
Tufts University, MA·Neuroscience
Test whether the ABCA7 p.Ala1527Gly variant lowers ABCA7 protein levels and causes loss of function in iPSC-derived human excitatory neurons, measuring Aβ42/40 ratios, a readout of harmful amyloid-β.
The school
University of South Florida: 20 labs on PI Pages, $522M a year on research, 305 research doctorates a year.
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