Steven Boeynaems
Baylor College of Medicine, TX·Neuroscience·Early-career
Neurodegenerative diseases damage more than neurons. They also inflame the brain, and glial cells, the support cells of the nervous system, drive part of this inflammation.
- Fields
Neuroscience
Microbiology & Immunology
Biophysics
- Topics
neuroinflammation
neurodegeneration
biomolecular condensates
- Grants
- 1 known grant, through Aug 2027
What they work on
- Define the biophysical rules by which neuropathological proteins form condensates with nucleic acids that mimic antimicrobial peptides and boost Toll-like receptor immune signaling, using in vitro biophysical approaches.
- Identify the signaling pathways through which condensates from ALS and frontotemporal dementia pathology activate the innate immune system, building on genetics- and proteomics-based screens.
- Test in in vivo disease models whether condensate-driven immune mimicry triggers neuroinflammation, and identify candidate targets and compounds for neuro-immunomodulation.
More about the research
These glia react to the clumps of misfolded protein that mark these diseases. That reaction is puzzling, because the immune system never evolved to detect diseases of old age. What it did evolve is ways to detect infection. This project asks whether disease proteins trigger inflammation by mimicking the signals of infection.
Why it matters
Brain inflammation strongly shapes how quickly neurodegenerative diseases such as ALS and frontotemporal dementia progress. Its molecular origins, however, are poorly understood. Identifying how disease protein condensates set off immune signaling could reveal new targets and compounds for calming harmful brain inflammation in these diseases.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Bruce Armitage
Carnegie Mellon University, PA·Chemistry
Design fluorescent peptide nucleic acid (PNA) probes that bind unmodified C9orf72 repeat RNAs, so these RNAs can be seen in biomolecular condensates by microscopy.
Jingjing Liang
University of Arizona, AZ·Neuroscience
Test how Aggregatin, a protein encoded by the Alzheimer's-linked gene FAM222A, controls TDP-43 clumping and toxicity in neurons, using Aggregatin knockout models.
Jailson Brito Querido
University of Michigan, MI·Biochemistry
Determine how expanded GGGGCC repeats in C9orf72 mRNA physically engage the ribosome to trigger non-AUG start site selection, using cryo-electron microscopy with biochemical and genetic approaches.
The school
Baylor College of Medicine: 38 labs on PI Pages, $881M a year on research, 115 research doctorates a year.
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